Subjects -> ENVIRONMENTAL STUDIES (Total: 965 journals)
    - ENVIRONMENTAL STUDIES (864 journals)
    - POLLUTION (29 journals)
    - TOXICOLOGY AND ENVIRONMENTAL SAFETY (55 journals)
    - WASTE MANAGEMENT (17 journals)

ENVIRONMENTAL STUDIES (864 journals)                  1 2 3 4 5 | Last

Showing 1 - 200 of 378 Journals sorted alphabetically
Acta Brasiliensis     Open Access   (Followers: 3)
Acta Ecologica Sinica     Open Access   (Followers: 11)
Acta Environmentalica Universitatis Comenianae     Open Access   (Followers: 1)
Acta Limnologica Brasiliensia     Open Access   (Followers: 4)
Acta Oecologica     Hybrid Journal   (Followers: 12)
Acta Regionalia et Environmentalica     Open Access   (Followers: 1)
Advanced Electronic Materials     Hybrid Journal   (Followers: 5)
Advanced Sustainable Systems     Hybrid Journal   (Followers: 5)
Advances in Ecological Research     Full-text available via subscription   (Followers: 45)
Advances in Environmental Chemistry     Open Access   (Followers: 10)
Advances in Environmental Sciences - International Journal of the Bioflux Society     Open Access   (Followers: 20)
Advances in Environmental Technology     Open Access   (Followers: 1)
Advances in Life Science and Technology     Open Access   (Followers: 22)
Advances in Tropical Biodiversity and Environmental Sciences     Open Access   (Followers: 3)
Aeolian Research     Hybrid Journal   (Followers: 6)
African Journal of Environmental Science and Technology     Open Access   (Followers: 5)
Agricultura Tecnica     Open Access   (Followers: 5)
Agricultural & Environmental Letters     Open Access   (Followers: 1)
Agro-Science     Full-text available via subscription   (Followers: 2)
Agroecological journal     Open Access  
Agronomy for Sustainable Development     Open Access   (Followers: 19)
Agrosystems, Geosciences & Environment     Open Access   (Followers: 3)
Amazon's Research and Environmental Law     Open Access   (Followers: 5)
Ambiência     Open Access  
Ambiens. Revista Iberoamericana Universitaria en Ambiente, Sociedad y Sustentabilidad     Open Access   (Followers: 1)
Ambiente & sociedade     Open Access   (Followers: 3)
Ambiente & Agua : An Interdisciplinary Journal of Applied Science     Open Access   (Followers: 1)
American Journal of Energy and Environment     Open Access   (Followers: 5)
American Journal of Environmental Engineering     Open Access   (Followers: 16)
American Journal of Environmental Protection     Open Access   (Followers: 9)
American Journal of Environmental Sciences     Open Access   (Followers: 11)
American Naturalist     Full-text available via subscription   (Followers: 82)
Annals of Civil and Environmental Engineering     Open Access   (Followers: 2)
Annals of Environmental Science and Toxicology     Open Access   (Followers: 3)
Annals of GIS     Hybrid Journal   (Followers: 23)
Annals of Warsaw University of Life Sciences ? SGGW. Land Reclamation     Open Access  
Annual Review of Ecology, Evolution, and Systematics     Full-text available via subscription   (Followers: 86)
Annual Review of Environment and Resources     Full-text available via subscription   (Followers: 16)
Annual Review of Pharmacology and Toxicology     Full-text available via subscription   (Followers: 35)
Annual Review of Resource Economics     Full-text available via subscription   (Followers: 10)
Applied and Environmental Soil Science     Open Access   (Followers: 20)
Applied Ecology and Environmental Sciences     Open Access   (Followers: 28)
Applied Environmental Education & Communication     Hybrid Journal   (Followers: 19)
Applied Journal of Environmental Engineering Science     Open Access   (Followers: 1)
Aquatic Ecology     Hybrid Journal   (Followers: 40)
Aquatic Toxicology     Hybrid Journal   (Followers: 24)
Arcada : Revista de conservación del patrimonio cultural     Open Access   (Followers: 1)
Architecture, Civil Engineering, Environment     Open Access   (Followers: 2)
Archives des Maladies Professionnelles et de l'Environnement     Full-text available via subscription  
Archives of Environmental and Occupational Health     Hybrid Journal   (Followers: 11)
Archives of Environmental Contamination and Toxicology     Hybrid Journal   (Followers: 14)
Archives of Environmental Protection     Open Access   (Followers: 6)
Archives of Toxicology     Hybrid Journal   (Followers: 20)
Arctic Environmental Research     Open Access   (Followers: 1)
Asia Pacific Journal of Environment Ecology and Sustainable Development     Open Access   (Followers: 7)
Asian Journal of Environment & Ecology     Open Access   (Followers: 1)
Asian Journal of Rural Development     Open Access   (Followers: 7)
Asian Review of Environmental and Earth Sciences     Open Access   (Followers: 2)
ATBU Journal of Environmental Technology     Open Access   (Followers: 5)
Atmospheric and Climate Sciences     Open Access   (Followers: 28)
Atmospheric Environment     Hybrid Journal   (Followers: 72)
Atmospheric Environment : X     Open Access   (Followers: 3)
Augm Domus : Revista electrónica del Comité de Medio Ambiente de AUGM     Open Access  
Austral Ecology     Hybrid Journal   (Followers: 16)
Australasian Journal of Environmental Management     Hybrid Journal   (Followers: 13)
Australasian Journal of Human Security     Full-text available via subscription   (Followers: 1)
Australian Journal of Environmental Education     Full-text available via subscription   (Followers: 10)
Basic & Clinical Pharmacology & Toxicology     Hybrid Journal   (Followers: 13)
Basic and Applied Ecology     Hybrid Journal   (Followers: 23)
Behavioral Ecology     Hybrid Journal   (Followers: 59)
Behavioral Ecology and Sociobiology     Hybrid Journal   (Followers: 38)
Biocenosis     Open Access  
Biochar     Hybrid Journal   (Followers: 3)
Biodegradation     Hybrid Journal   (Followers: 1)
Biodiversity     Hybrid Journal   (Followers: 27)
Biofouling: The Journal of Bioadhesion and Biofilm Research     Hybrid Journal   (Followers: 7)
Bioremediation Journal     Hybrid Journal   (Followers: 5)
BioRisk     Open Access   (Followers: 3)
BMC Ecology     Open Access   (Followers: 24)
Boletín Instituto de Derecho Ambiental y de los Recursos Naturales     Open Access  
Boletín Semillas Ambientales     Open Access  
Boston College Environmental Affairs Law Review     Open Access   (Followers: 7)
Bothalia : African Biodiversity & Conservation     Open Access   (Followers: 1)
Built Environment     Full-text available via subscription   (Followers: 4)
Bulletin of Environmental Contamination and Toxicology     Hybrid Journal   (Followers: 15)
Bulletin of the American Meteorological Society     Open Access   (Followers: 49)
Bumi Lestari Journal of Environment     Open Access  
Business, Peace and Sustainable Development     Full-text available via subscription   (Followers: 8)
Canadian Journal of Earth Sciences     Hybrid Journal   (Followers: 23)
Canadian Journal of Remote Sensing     Full-text available via subscription   (Followers: 46)
Canadian Journal of Soil Science     Full-text available via subscription   (Followers: 14)
Canadian Water Resources Journal     Hybrid Journal   (Followers: 20)
Capitalism Nature Socialism     Hybrid Journal   (Followers: 26)
Carbon Resources Conversion     Open Access   (Followers: 1)
Casopis Slezskeho Zemskeho Muzea - serie A - vedy prirodni     Open Access  
Cell Biology and Toxicology     Hybrid Journal   (Followers: 13)
Chain Reaction     Full-text available via subscription  
Challenges in Sustainability     Open Access   (Followers: 8)
Change and Adaptation in Socio-Ecological Systems     Open Access   (Followers: 4)
Chemical Research in Toxicology     Hybrid Journal   (Followers: 25)
Chemico-Biological Interactions     Hybrid Journal   (Followers: 3)
Chemosphere     Hybrid Journal   (Followers: 16)
Child and Adolescent Mental Health     Hybrid Journal   (Followers: 71)
China Population, Resources and Environment     Full-text available via subscription   (Followers: 4)
Chinese Journal of Environmental Law     Hybrid Journal   (Followers: 1)
Ciencia, Ambiente y Clima     Open Access   (Followers: 3)
City and Environment Interactions     Open Access   (Followers: 2)
Civil and Environmental Engineering     Open Access   (Followers: 8)
Civil and Environmental Engineering Reports     Open Access   (Followers: 9)
Civil and Environmental Research     Open Access   (Followers: 19)
CLEAN - Soil, Air, Water     Hybrid Journal   (Followers: 21)
Clean Technologies     Open Access  
Clean Technologies and Environmental Policy     Hybrid Journal   (Followers: 5)
Cleanroom Technology     Full-text available via subscription   (Followers: 1)
Climate Change Economics     Hybrid Journal   (Followers: 14)
Climate Policy     Hybrid Journal   (Followers: 36)
Coastal Engineering Journal     Hybrid Journal   (Followers: 7)
Cogent Environmental Science     Open Access  
Columbia Journal of Environmental Law     Open Access   (Followers: 14)
Computational Ecology and Software     Open Access   (Followers: 11)
Computational Water, Energy, and Environmental Engineering     Open Access   (Followers: 5)
Conservation and Society     Open Access   (Followers: 10)
Conservation Letters     Open Access   (Followers: 45)
Conservation Science     Open Access   (Followers: 25)
Consilience : The Journal of Sustainable Development     Open Access   (Followers: 1)
Contemporary Problems of Ecology     Hybrid Journal   (Followers: 4)
Critical Reviews in Environmental Science and Technology     Hybrid Journal   (Followers: 14)
Critical Reviews in Toxicology     Hybrid Journal   (Followers: 25)
Cuadernos de Investigación Geográfica / Geographical Research Letters     Open Access  
Culture, Agriculture, Food and Environment     Hybrid Journal   (Followers: 20)
Culture, Agriculture, Food and Environment     Hybrid Journal   (Followers: 9)
Current Environmental Engineering     Hybrid Journal  
Current Environmental Health Reports     Hybrid Journal   (Followers: 1)
Current Forestry Reports     Hybrid Journal   (Followers: 1)
Current Landscape Ecology Reports     Hybrid Journal   (Followers: 2)
Current Opinion in Environmental Science & Health     Hybrid Journal   (Followers: 1)
Current Opinion in Environmental Sustainability     Hybrid Journal   (Followers: 15)
Current Research in Microbiology     Open Access   (Followers: 25)
Current Sustainable/Renewable Energy Reports     Hybrid Journal   (Followers: 7)
Current World Environment     Open Access   (Followers: 4)
Developments in Atmospheric Science     Full-text available via subscription   (Followers: 27)
Developments in Earth and Environmental Sciences     Full-text available via subscription   (Followers: 3)
Developments in Earth Surface Processes     Full-text available via subscription   (Followers: 1)
Developments in Environmental Modelling     Full-text available via subscription   (Followers: 8)
Developments in Environmental Science     Full-text available via subscription   (Followers: 3)
Developments in Integrated Environmental Assessment     Full-text available via subscription   (Followers: 4)
Die Bodenkultur: Journal of Land Management, Food and Environment     Open Access  
disP - The Planning Review     Hybrid Journal  
Divulgación Científica     Open Access   (Followers: 1)
Drug and Chemical Toxicology     Hybrid Journal   (Followers: 16)
Duke Environmental Law & Policy Forum     Open Access   (Followers: 6)
Dynamiques Environnementales     Open Access   (Followers: 3)
E3S Web of Conferences     Open Access   (Followers: 2)
Earth and Environmental Science Transactions of the Royal Society of Edinburgh     Hybrid Journal   (Followers: 6)
Earth Interactions     Open Access   (Followers: 12)
Earth Science Informatics     Hybrid Journal   (Followers: 4)
Earth System Governance     Open Access  
Earth System Science Data (ESSD)     Open Access   (Followers: 7)
Earth System Science Data Discussions (ESSDD)     Open Access   (Followers: 4)
Earth Systems and Environment     Hybrid Journal   (Followers: 2)
Earthquake Science     Hybrid Journal   (Followers: 13)
EchoGéo     Open Access  
Eco-Thinking     Open Access   (Followers: 4)
Ecocycles     Open Access   (Followers: 6)
Ecohydrology     Hybrid Journal   (Followers: 10)
Ecohydrology & Hydrobiology     Full-text available via subscription   (Followers: 3)
Ecologia Aplicada     Open Access  
Ecología en Bolivia     Open Access  
Ecological Applications     Full-text available via subscription   (Followers: 202)
Ecological Chemistry and Engineering S     Open Access   (Followers: 4)
Ecological Complexity     Hybrid Journal   (Followers: 7)
Ecological Engineering     Hybrid Journal   (Followers: 4)
Ecological Engineering : X     Open Access  
Ecological Indicators     Hybrid Journal   (Followers: 20)
Ecological Informatics     Hybrid Journal   (Followers: 4)
Ecological Management & Restoration     Hybrid Journal   (Followers: 15)
Ecological Modelling     Hybrid Journal   (Followers: 96)
Ecological Monographs     Full-text available via subscription   (Followers: 39)
Ecological Processes     Open Access   (Followers: 1)
Ecological Questions     Open Access   (Followers: 4)
Ecological Research     Hybrid Journal   (Followers: 10)
Ecological Restoration     Full-text available via subscription   (Followers: 22)
Ecologist, The     Full-text available via subscription   (Followers: 22)
Ecology     Full-text available via subscription   (Followers: 456)
Ecology and Evolution     Open Access   (Followers: 94)
Ecology Letters     Hybrid Journal   (Followers: 337)
EcoMat : Functional Materials for Green Energy and Environment     Open Access   (Followers: 5)
Economics and Policy of Energy and the Environment     Full-text available via subscription   (Followers: 13)
Économie rurale     Open Access   (Followers: 3)
Ecoprint : An International Journal of Ecology     Open Access   (Followers: 6)
Ecopsychology     Hybrid Journal   (Followers: 8)
Ecosphere     Open Access   (Followers: 9)
Ecosystem Services     Hybrid Journal   (Followers: 10)
Ecosystems     Hybrid Journal   (Followers: 33)
Ecosystems and People     Open Access   (Followers: 1)
Ecotoxicology     Hybrid Journal   (Followers: 11)
Ecotoxicology and Environmental Safety     Hybrid Journal   (Followers: 11)
Ecotrophic : Journal of Environmental Science     Open Access  
Ecozon@ : European Journal of Literature, Culture and Environment     Open Access   (Followers: 5)
Éducation relative à l'environnement     Open Access  

        1 2 3 4 5 | Last

Similar Journals
Journal Cover
Cell Biology and Toxicology
Journal Prestige (SJR): 0.924
Citation Impact (citeScore): 5
Number of Followers: 13  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1573-6822 - ISSN (Online) 0742-2091
Published by Springer-Verlag Homepage  [2626 journals]
  • High-content screening of diterpenoids from Isodon species as autophagy
           modulators and the functional study of their antiviral activities
    • Abstract: Autophagy is a conserved lysosomal degradation process, and abnormal autophagy has been associated with various pathological processes, e.g., neurodegeneration, cancer, and pathogen infection. Small chemical modulators of autophagy show the potential to treat autophagy-associated diseases. Diterpenoids, nature products found in various plants, exhibit a wide range of bioactivity, and we have recently isolated and characterized over 150 diterpenoids from Isodon species distributed in China. Here, we applied a high-content fluorescence imaging-based assay to assess these diterpenoids’ ability to affect autophagic flux in HeLa cells. We found that enanderinanin J, an ent-kauranoid dimer, is an autophagy inhibitor, manifested by its ability to increase lysosomal pH and inhibit the fusion between autophagosomes and lysosomes. Autophagy has been shown to be either positively or negatively involved in the life cycle of Zika virus (ZIKV), Japanese encephalitis virus (JEV), Dengue virus (DENV), and enterovirus-A71 (EV-A71). We found that enanderinanin J significantly inhibited the infection of ZIKV, DENV, JEV, or EV-A71. Interestingly, although ATG5 knockdown inhibited ZIKV or JEV infection, enanderinanin J further inhibited the infection of ZIKV or JEV in ATG5-knockdown cells. Taken together, our data indicate that enanderinanin J inhibits autophagosome-lysosome fusion and is a potential antiviral agent. Graphical abstract
      PubDate: 2021-01-23
       
  • MC-LR-induced interaction between M2 macrophage and biliary epithelial
           cell promotes biliary epithelial cell proliferation and migration through
           regulating STAT3
    • Abstract: Microcystin-leucine-arginine (MC-LR) was produced by toxic cyanobacteria, which has been shown to have potent hepatotoxicity. Our previous study has proved that MC-LR were able to promote intrahepatic biliary epithelial cell excessive proliferation. However, the underlying mechanism is not yet entirely clarified. Herein, mice were fed with different concentrations (1, 7.5, 15, or 30 μg/L) of MC-LR by drinking water for 6 months. As the concentration of MC-LR increased, a growing number of macrophages were evaluated in the portal area of the mouse liver. Next, we built a co-culture system to explore the interaction between macrophages (THP-1 cells) and human intrahepatic biliary epithelial cells (HiBECs) in the presence of MC-LR. Under the exposure of MC-LR, HiBECs secreted a large amount of inflammatory factors (IL-6, IL-8, IL-1β, COX-2, XCL-1) and chemokine (MCP-1), which produced a huge chemotactic effect on THP-1 cells and induced elevation of the surface M2-subtype biomarkers (IL-10, CD163, CCL22, and Arg-1). In turn, high content of IL-6 in the medium activated JAK2/STAT3, MEK/ERK, and PI3K/AKT pathways in HiBECs, inducing HiBEC abnormal proliferation and migration. Together, these results suggested that MC-LR-mediated interaction between HiBECs and macrophages induced the M2-type polarization of macrophages, and activated IL-6/JAK2/STAT3, MEK/ERK, and PI3K/AKT pathways in HiBECs, further enhanced cell proliferation, improved cell migration, and hindered cell apoptosis by activating p-STAT3. Graphical abstract MC-LR stimulates HiBECs to produce various inflammatory factors, recruiting a large number of macrophages and promoting the differentiation of macrophages into M2-type. In turn, the M2 macrophages could also produce amounts of IL-6 and activate STAT3 through JAK2/STAT3, MEK/ERK, and PI3K/AKT pathways in HiBECs, resulting in the promotion of cell proliferation, inhibition of apoptosis, and enhancement of migration.
      PubDate: 2021-01-21
       
  • E-cig vapor condensate alters proteome and lipid profiles of membrane
           rafts: impact on inflammatory responses in A549 cells
    • Abstract: Abstract Electronic cigarettes (e-cigs) are battery-operated heating devices that aerosolize e-liquid, typically containing nicotine and several other chemicals, which is then inhaled by a user. Over the past decade, e-cigs have gained immense popularity among both smokers and non-smokers. One reason for this is that they are advertised as a safe alternative to conventional cigarettes. However, the recent reports of e-cig use associated lung injury have ignited a considerable debate about the relative harm and benefits of e-cigs. The number of reports about e-cig-induced inflammation and pulmonary health is increasing as researchers seek to better understand the effects of vaping on human health. In line with this, we investigated the molecular events responsible for the e-cig vapor condensate (ECVC)–mediated inflammation in human lung adenocarcinoma type II epithelial cells (A549). In an attempt to limit the variables caused by longer ingredient lists of flavored e-cigs, tobacco-flavored ECVC (TF-ECVC±nicotine) was employed for this study. Interestingly, we observed significant upregulation of cytokines and chemokines (IL-6, IL-8, and MCP-1) in A549 cells following a 48 h TF-ECVC challenge. Furthermore, there was a significant increase in the expression of pattern recognition receptors TLR-4 and NOD-1, lipid raft–associated protein caveolin-1, and transcription factor NF-кB in TF-ECVC with and/or without nicotine-challenged lung epithelial cells. Our results further demonstrate the harboring of TLR-4 and NOD-1 in the caveolae of TF-ECVC-challenged A549 cells. Proteomic and lipidomic analyses of lipid raft fractions from control and challenged cells revealed a distinct protein and lipid profile in TF-ECVC (w/wo nicotine)-exposed A549 cells. Interestingly, the inflammatory effects of TF-ECVC (w/wo nicotine) were inhibited following the caveolin-1 knockdown, thus demonstrating a critical role of caveolae raft–mediated signaling in eliciting inflammatory responses upon TF-ECVC challenge. Graphical Abstract Graphical Abstract
      PubDate: 2021-01-20
       
  • Endothelial ERG alleviates cardiac fibrosis via blocking
           endothelin-1-dependent paracrine mechanism
    • Abstract: Cardiac endothelium communicates closely with adjacent cardiac cells by multiple cytokines and plays critical roles in regulating fibroblasts proliferation, activation, and collagen synthesis during cardiac fibrosis. E26 transformation-specific (ETS)-related gene (ERG) belongs to the ETS transcriptional factor family and is required for endothelial cells (ECs) homeostasis and cardiac development. This study aims at investigating the potential role and molecular basis of ERG in fibrotic remodeling within the adult heart. We observed that ERG was abundant in murine hearts, especially in cardiac ECs, but decreased during cardiac fibrosis. ERG knockdown within murine hearts caused spontaneously cardiac fibrosis and dysfunction, accompanied by the activation of multiple Smad-dependent and independent pathways. However, the direct silence of ERG in cardiac fibroblasts did not affect the expression of fibrotic markers. Intriguingly, ERG knockdown in human umbilical vein endothelial cells (HUVECs) promoted the secretion of endothelin-1 (ET-1), which subsequently accelerated the proliferation, phenotypic transition, and collagen synthesis of cardiac fibroblasts in a paracrine manner. Suppressing ET-1 with either a neutralizing antibody or a receptor blocker abolished ERG knockdown-mediated deleterious effect in vivo and in vitro. This pro-fibrotic effect was also negated by RGD (Arg-Gly-Asp)-peptide magnetic nanoparticles target delivery of ET-1 small interfering RNA to ECs in mice. More importantly, we proved that endothelial ERG overexpression notably prevented pressure overload-induced cardiac fibrosis. Collectively, endothelial ERG alleviates cardiac fibrosis via blocking ET-1-dependent paracrine mechanism and it functions as a candidate for treating cardiac fibrosis. Graphical abstract • ERG is abundant in murine hearts, especially in cardiac ECs, but decreased during fibrotic remodeling. • ERG knockdown causes spontaneously cardiac fibrosis and dysfunction. • ERG silence in HUVECs promotes the secretion of endothelin-1, which in turn activates cardiac fibroblasts in a paracrine manner. • Endothelial ERG overexpression prevents pressure overload-induced cardiac fibrosis.
      PubDate: 2021-01-20
       
  • Sclareol inhibits RANKL-induced osteoclastogenesis and promotes
           osteoblastogenesis through promoting CCN1 expression via repressing the
           MAPK pathway
    • Abstract: Osteoclasts are crucial cellular components of bone and are the cause of various bone problems like osteoporosis. Various biological activities such as anti-tumorous, anti-inflammatory, antibacterial, and immunomodulatory function are influenced by Sclareol, as a natural diterpene compound. However, studies on the effect and mechanism of Sclareol on osteoporosis are rare. In the current research, the influence of Sclareol on osteoclastogenesis and osteoblastogenesis was targeted to be discovered in ovariectomy (OVX)-induced animal models and in vitro. The expression levels of osteoclast-related genes such as c-Fos, NFATc1, and CTSK were detected by RT-qPCR and western blotting to understand the inhibition of Sclareol on the creation of osteoclast. The influence of Sclareol on osteoblastogenesis and the expression of osteoblastogenic markers were also examined. Sclareol inhibited the osteoclastogenesis caused by receptor activator of nuclear factor-κB ligand (RANKL) which promoted osteoblastogenesis through upregulating the expression of cysteine-rich protein 61 (CYR61/CCN1), which is a matricellular protein of the CCN family. The p-ERK and p-P38 protein expression levels were considerably downregulated by Sclareol. Furthermore, CCN1 overexpression partially mimicked the inhibitory effect of Sclareol, while the opposite results were obtained after CCN1 silencing. Additionally, Sclareol protected against loss of bones in an osteoporosis mouse model generated by OVX. The acquired results indicated that Sclareol represses RANKL-induced osteoclastogenesis and promotes osteoblastogenesis via promoting the expression of CCN1 by constraining the mitogen-activated protein kinase (MAPK) pathway. Our findings proposed that for the avoidance and treatment of osteoclast-linked disorders, Sclareol is a potentially effective drug. Graphical abstract A proposed model for mediated regulation of osteoclastogenesis and osteoblastogenesis by Sclareol. The basic model of the process by which Sclareol prevents osteoclastogenesis and promotes osteoblastogenesis. Sclareol may increase the expression of CCN1 through inhibiting the MAPK pathway, thereby inhibiting osteoclast differentiation and attenuating bone resorption. Sclareol represses the expression of c-Fos, which stimulates the formation of osteoclast. In contrast, Sclareol promotes osteoblast differentiation by upregulating Runx2 expression, thereby improving the formation of bones. Consequently, Sclareol protects against loss of bones by regulating the stability of bone makeover via inhibition of bone formation and stimulation of bone resorption. Graphical Headlights 1. Sclareol represses RANKL-induced osteoclastogenesis. 2. Sclareol promotes osteoblast differentiation. 3. Sclareol inhibits the MAPK pathway through induction of CCN1. 4. Sclareol protects against bone loss by regulating the balance of bone remodeling via inhibition of bone formation and stimulation of bone resorption.
      PubDate: 2021-01-09
       
  • Biophysical phenotyping of mesenchymal stem cells along the osteogenic
           differentiation pathway
    • Abstract: Abstract Mesenchymal stem cells represent an important resource, for bone regenerative medicine and therapeutic applications. This review focuses on new advancements and biophysical tools which exploit different physical and chemical markers of mesenchymal stem cell populations, to finely characterize phenotype changes along their osteogenic differentiation process. Special attention is paid to recently developed label-free methods, which allow monitoring cell populations with minimal invasiveness. Among them, quantitative phase imaging, suitable for single-cell morphometric analysis, and nanoindentation, functional to cellular biomechanics investigation. Moreover, the pool of ion channels expressed in cells during differentiation is discussed, with particular interest for calcium homoeostasis.Altogether, a biophysical perspective of osteogenesis is proposed, offering a valuable tool for the assessment of the cell stage, but also suggesting potential physiological links between apparently independent phenomena.
      PubDate: 2021-01-09
       
  • Benzo(a)pyrene-induced cytotoxicity, cell proliferation, DNA damage, and
           altered gene expression profiles in HT-29 human colon cancer cells
    • Abstract: In the US alone, around 60,000 lives/year are lost to colon cancer. In order to study the mechanisms of colon carcinogenesis, in vitro model systems are required in addition to in vivo models. Towards this end, we have used the HT-29 colon cancer cells, cultured in Dulbecco’s Modified Eagle Medium (DMEM), which were exposed to benzo(a)pyrene (BaP), a ubiquitous and prototypical environmental and dietary toxicant at 1, 10, 100 nM and 1, 5, 10, and 25 μM concentrations for 96 h. Post-BaP exposure, growth, cytotoxicity, apoptosis, and cell cycle changes were determined. The BaP metabolite concentrations in colon cells were identified and measured. Furthermore, the BaP biotransformation enzymes were studied at the protein and mRNA levels. The BaP exposure–induced damage to DNA was assessed by measuring the oxidative damage to DNA and the concentrations of BaP-DNA adducts. To determine the whole repertoire of genes that are up- or downregulated by BaP exposure, mRNA transcriptome analysis was conducted. There was a BaP exposure concentration (dose)-dependent decrease in cell growth, cytotoxicity, and modulation of the cell cycle in the treatment groups compared to untreated or dimethylsulfoxide (DMSO: vehicle for BaP)-treated categories. The phase I biotransformation enzymes, CYP1A1 and 1B1, showed BaP concentration-dependent expression. On the other hand, phase II enzymes did not exhibit any marked variation. Consistent with the expression of phase I enzymes, elevated concentrations of BaP metabolites were generated, contributing to the formation of DNA lesions and stable DNA adducts, which were also BaP concentration-dependent. In summary, our studies established that biotransformation of BaP contributes to cytotoxicity, proliferation of tumor cells, and alteration of gene expression by BaP. Graphical abstract • Benzo(a)pyrene (BaP) is an environmental and dietary toxicant. • BaP causes cytotoxicity in cultured HT-29 colon cancer cells. • mRNA transcriptome analyses revealed that BaP impacts cell growth, cell cycle, biotransformation, and DNA damage.
      PubDate: 2021-01-07
       
  • Implant-derived CoCrMo alloy nanoparticle disrupts DNA replication
           dynamics in neuronal cells
    • Abstract: The complexity of cobalt-chromium-molybdenum (CoCrMo) nanoparticles generated from the hip modular taper interfaces resulted in inconclusive outcomes on the level of toxicity in orthopedic patients. We used a hip simulator to generate physiologically relevant CoCrMo degradation products (DPs) to demonstrate the variation in the level of toxicity in neurons in comparison to processed degradation products (PDPs). The study outcomes indicate that DP induces a higher level of DNA damage in the form of double- and single-stranded DNA breaks and alkaline labile DNA adducts versus PDPs. The scientific advancements of this study are the following: (i) how DPs mimic more closely to the implant debris from hip implants in terms of bioactivity, (ii) how hip implant debris causes local and systemic issues, and (iii) methods to augment the biologic impact of implant debris. We discovered that DP is bioactive compared with PDP, and this should be considered in the toxicity evaluation related to implants. Graphical abstract • The physicochemical characteristics of the CoCrMo is a major factor to consider for implant-related cytotoxicity or genotoxicity experimental design. • Elevated levels of intracellular ROS induced by the physiologically relevant wear particle are detrimental to the neuronal cells. • The DP can induce variation in DNA replication dynamics compared to PDP.
      PubDate: 2021-01-07
       
  • A multi-omic study for uncovering molecular mechanisms associated with
           hyperammonemia-induced cerebellar function impairment in rats
    • Abstract: Abstract Patients with liver cirrhosis may develop covert or minimal hepatic encephalopathy (MHE). Hyperammonemia (HA) and peripheral inflammation play synergistic roles in inducing the cognitive and motor alterations in MHE. The cerebellum is one of the main cerebral regions affected in MHE. Rats with chronic HA show some motor and cognitive alterations reproducing neurological impairment in cirrhotic patients with MHE. Neuroinflammation and altered neurotransmission and signal transduction in the cerebellum from hyperammonemic (HA) rats are associated with motor and cognitive dysfunction, but underlying mechanisms are not completely known. The aim of this work was to use a multi-omic approach to study molecular alterations in the cerebellum from hyperammonemic rats to uncover new molecular mechanisms associated with hyperammonemia-induced cerebellar function impairment. We analyzed metabolomic, transcriptomic, and proteomic data from the same cerebellums from control and HA rats and performed a multi-omic integrative analysis of signaling pathway enrichment with the PaintOmics tool. The histaminergic system, corticotropin-releasing hormone, cyclic GMP-protein kinase G pathway, and intercellular communication in the cerebellar immune system were some of the most relevant enriched pathways in HA rats. In summary, this is a good approach to find altered pathways, which helps to describe the molecular mechanisms involved in the alteration of brain function in rats with chronic HA and to propose possible therapeutic targets to improve MHE symptoms.
      PubDate: 2021-01-06
       
  • SEW2871 attenuates ANIT-induced hepatotoxicity by protecting liver barrier
           function via sphingosine 1-phosphate receptor-1–mediated AMPK signaling
           pathway
    • Abstract: Cholestatic liver injury, a group of diseases characterized with dysregulated bile acid (BA) homeostasis, was partly resulted from BA circulation disorders, which is commonly associated with the damage of hepatocyte barrier function. However, the underlying hepatocyte barrier-protective molecular mechanisms of cholestatic liver injury remain poorly understood. Interestingly, recent studies have shown that sphingosine-1-phosphate (S1P) participated in the process of cholestasis by activating its G protein–coupled receptors S1PRs, regaining the integrity of hepatocyte tight junctions (TJs). Here, we showed that SEW2871, a selective agonist of sphingosine-1-phosphate receptor 1(S1PR1), alleviated ANIT–induced TJs damage in 3D-cultured mice primary hepatocytes. Molecular mechanism studies indicated that AMPK signaling pathways was involved in TJs protection of SEW2871 in ANIT-induced hepatobiliary barrier function deficiency. AMPK antagonist compound C (CC) and agonist AICAR were all used to further identify the important role of AMPK signaling pathway in SEW2871’s TJs protection of ANIT-treated mice primary hepatocytes. The in vivo data showed that SEW2871 ameliorated ANIT-induced cholestatic hepatotoxicity. Further protection mechanism research demonstrated that SEW2871 not only regained hepatocyte TJs by the upregulated S1PR1 via AMPK signaling pathway, but also recovered hepatobiliary barrier function deficiency, which was verified by the restored BA homeostasis by using of high-performance liquid chromatography-tandem mass spectrometry (LC-MS/MS). These results revealed that the increased expression of S1PR1 induced by SEW2871 could ameliorate ANIT–induced cholestatic liver injury through improving liver barrier function via AMPK signaling and subsequently reversed the disrupted BA homeostasis. Our study provided strong evidence that S1PR1 may be a promising therapeutic approach for treating intrahepatic cholestatic liver injury. Graphical abstract
      PubDate: 2021-01-05
       
  • Up-regulation of the expressions of MiR-149-5p and MiR-99a-3p in exosome
           inhibits the progress of pituitary adenomas
    • Abstract: This study explored the function of microRNAs (miRNAs) in invasive pituitary adenomas (IPA), and developed a microRNA-exosome strategy for the disease treatment. Differentially expressed miRNAs and tumor-associated markers in IPA, non-invasive pituitary adenoma (NIPA), and rat pituitary adenoma cells were identified by bioinformatics analysis and qRT-PCR. Then, the cells were treated by miR-149-5p and miR-99a-3p mimics or inhibitors, or incubated with modified exosome with overexpressed or silenced miRNAs. The cell behaviors were analyzed by molecular experiments. Xenograft assays were constructed by injection of pituitary adenoma cells and exosome into NU/NU nude mice. Tumor size, weight, and expressions of markers related to miRNAs and angiogenesis were determined. Target genes for miR-99a-3p and miR-149 were predicted and verified by bioinformatics analysis and molecular experiments. Twenty differentially expressed miRNAs were identified, among which miR-99a-3p and miR-149 were inhibited in both pituitary adenoma cells and tissues significantly. Expressions of E-cadherin and p53 were down-regulated, while those of MMP-2, MMP-9, N-cadherin, Vimentin, and VEGF were up-regulated in pituitary adenoma cells and tissues, especially in IPA. Further experiments revealed that overexpressed miR-149 and miR-99a-3p inhibited the growth and metastasis of pituitary adenoma cells and tube formation of endothelial cells. MiR-149 and miR-99a-3p overexpressed by exosome showed similar suppressive effects on cell viability, metastasis, tube formation ability, in vivo tumor growth, and expressions of angiogenesis-related markers. Further analysis showed that NOVA1, DTL, and RAB27B were targeted by miR-99a-3p. This study found that overexpressed miR-149-5p and miR-99a-3p induced by exosome could suppress the progression of IPA. Graphical abstract and graphical headlights 1. MiR-149-5p and miR-99a-3p affect the expression of EMT- and ECM-related markers and tumor-related genes in rat pituitary adenoma cells treated with exosomes. 2. Exosome inhibited the tumor growth. 3. Overexpressed miR-149-5p and miR-99a-3p induced by exosome
      PubDate: 2021-01-05
       
  • Significance of single-cell and spatial transcriptomes in cell biology and
           toxicology
    • PubDate: 2021-01-04
       
  • S100A16 promotes metastasis and progression of pancreatic cancer through
           FGF19-mediated AKT and ERK1/2 pathways
    • Abstract: The S100 protein family genes play a crucial role in multiple stages of tumorigenesis and progression. Most of S100 genes are located at chromosome locus 1q21, which is a region frequently rearranged in cancers. Here, we examined the expression of the S100 family genes in paired pancreatic ductal adenocarcinoma (PDAC) samples and further validated the expression of S100A16 by immunohistochemistry staining. We found that S100A16 is significantly upregulated in clinical PDAC samples. However, its roles in PDAC are still unclear. We next demonstrated that S100A16 promotes PDAC cell proliferation, migration, invasion, and metastasis both in vitro and in vivo. Knockdown of S100A16 induces PDAC cell cycle arrest in the G2/M phase and apoptosis. Furthermore, we also demonstrated that S100A16 promotes PDAC cell proliferation, migration, and invasion via AKT and ERK1/2 signaling in a fibroblast growth factor 19 (FGF19)-dependent manner. Taken together, our results reveal that S100A16 is overexpressed in PDAC and promotes PDAC progression through FGF19-mediated AKT and ERK1/2 signaling, suggesting that S100A16 may be a promising therapeutic target for PDAC. Graphical abstract S100A16 was upregulated in PDAC and associated with prognosis of PDAC patients. S100A16 regulates apoptosis and the cell cycle of pancreatic cancer cells. S100A16 promotes the progression of pancreatic cancer by AKT-ERK1/2 signaling. S100A16 may be a promising therapeutic target for PDAC.
      PubDate: 2021-01-02
       
  • Correction to: Cytoplasmic sirtuin 6 translocation mediated by p62
           polyubiquitination plays a critical role in cadmium-induced kidney
           toxicity
    • Abstract: In the original publication the grant number is incorrectly published.
      PubDate: 2020-12-01
       
  • Ion transport mechanisms for smoke inhalation–injured airway
           epithelial barrier
    • Abstract: Smoke inhalation injury is the leading cause of death in firefighters and victims. Inhaled hot air and toxic smoke are the predominant hazards to the respiratory epithelium. We aimed to analyze the effects of thermal stress and smoke aldehyde on the permeability of the airway epithelial barrier. Transepithelial resistance (RTE) and short-circuit current (ISC) of mouse tracheal epithelial monolayers were digitized by an Ussing chamber setup. Zonula occludens-1 tight junctions were visualized under confocal microscopy. A cell viability test and fluorescein isothiocyanate-dextran assay were performed. Thermal stress (40 °C) decreased RTE in a two-phase manner. Meanwhile, thermal stress increased ISC followed by its decline. Na+ depletion, amiloride (an inhibitor for epithelial Na+ channels [ENaCs]), ouabain (a blocker for Na+/K+-ATPase), and CFTRinh-172 (a blocker of cystic fibrosis transmembrane regulator [CFTR]) altered the responses of RTE and ISC to thermal stress. Steady-state 40 °C increased activity of ENaCs, Na+/K+-ATPase, and CFTR. Acrolein, one of the main oxidative unsaturated aldehydes in fire smoke, eliminated RTE and ISC. Na+ depletion, amiloride, ouabain, and CFTRinh-172 suppressed acrolein-sensitive ISC, but showed activating effects on acrolein-sensitive RTE. Thermal stress or acrolein disrupted zonula occludens-1 tight junctions, increased fluorescein isothiocyanate-dextran permeability but did not cause cell death or detachment. The synergistic effects of thermal stress and acrolein exacerbated the damage to monolayers. In conclusion, the paracellular pathway mediated by the tight junctions and the transcellular pathway mediated by active and passive ion transport pathways contribute to impairment of the airway epithelial barrier caused by thermal stress and acrolein. Graphical abstract Thermal stress and acrolein are two essential determinants for smoke inhalation injury, impairing airway epithelial barrier. Transcellular ion transport pathways via the ENaC, CFTR, and Na/K-ATPase are interrupted by both thermal stress and acrolein, one of the most potent smoke toxins. Heat and acrolein damage the integrity of the airway epithelium through suppressing and relocating the tight junctions.
      PubDate: 2020-12-01
       
  • Drug efficacy and toxicity prediction: an innovative application of
           transcriptomic data
    • Abstract: Abstract Drug toxicity and efficacy are difficult to predict partly because they are both poorly defined, which I aim to remedy here from a transcriptomic perspective. There are two major categories of drugs: (1) restorative drugs aiming to restore an abnormal cell, tissue, or organ to normal function (e.g., restoring normal membrane function of epithelial cells in cystic fibrosis), and (2) disruptive drugs aiming to kill pathogens or malignant cells. These two types of drugs require different definition of efficacy and toxicity. I outlined rationales for defining transcriptomic efficacy and toxicity and illustrated numerically their application with two sets of transcriptomic data, one for restorative drugs (treating cystic fibrosis with lumacaftor/ivacaftor aiming to restore the cellular function of epithelial cells) and the other for disruptive drugs (treating acute myeloid leukemia with prexasertib). The conceptual framework presented will help and sensitize researchers to collect data required for determining drug toxicity.
      PubDate: 2020-12-01
       
  • Pulsed laser deposition temperature effects on strontium-substituted
           hydroxyapatite thin films for biomedical implants
    • Abstract: Abstract Substituting small molecule drugs with abundant and easily affordable ions may have positive effects on the way countless disease treatments are approached. The interest in strontium cation in bone therapies soared in the wake of the success of strontium ranelate in the treatment of osteoporosis. A new method for producing thin strontium-containing hydroxyapatite (Sr-HA, Ca9Sr(PO4)6(OH)2) films as coatings that render bioinert titanium implant bioactive is reported here. The method is based on the combination of a mechanochemical synthesis of Sr-HA targets and their deposition in form of thin films on top of titanium with the use of laser ablation at low pressure. The films were 1–2 μm in thickness and their formation was studied at different temperatures, including 25, 300, and 500 °C. Highly crystalline Sr-HA target transformed during pulsed laser deposition to a fully amorphous film, whose degree of long-range order recovered with temperature. Particle edges became somewhat sharper and surface roughness moderately increased with temperature, but the (Ca+Sr)/P atomic ratio, which increased 1.5 times during the film formation, remained approximately constant at different temperatures. Despite the mostly amorphous structure of the coatings, their affinity for capturing atmospheric carbon dioxide and accommodating it as carbonate ions that replace both phosphates and hydroxyls of HA was confirmed in an X-ray photoelectron spectroscopic analysis. As the film deposition temperature increased, the lattice voids got reduced in concentration and the structure gradually “closed,” becoming more compact and entailing a linear increase in microhardness with temperature, by 0.03 GPa/°C for the entire 25–500 °C range. Biocompatibility and bioactivity of Sr-HA thin films deposited on titanium were confirmed in an interaction with dental pulp stem cells, suggesting that these coatings, regardless of the processing temperature, may be viable candidates for the surface components of metallic bone implants.
      PubDate: 2020-12-01
       
  • Autophagy-mediating microRNAs in cancer chemoresistance
    • Abstract: Abstract Chemoresistance is a complex phenomenon responsible for failure in response to chemotherapy agents and more than 90% of deaths in cancer patients. MicroRNAs (miRNAs), as a subgroup of non-coding RNAs with lengths between 21 and 25 nucleotides, are involved in various cancer processes like chemoresistance via interacting with their target mRNAs and suppressing their expression. Autophagy is a greatly conserved procedure involving the lysosomal degradation of cytoplasmic contents and organelles to deal with environmental stresses like hypoxia and starvation. Autophagy contributes to response to chemotherapy agents: autophagy can act as a protective mechanism for mediating the resistance in response to chemotherapy or can induce autophagic cell death and mediate the sensitivity to chemotherapy. On the other hand, one of the processes targeted by microRNAs in the regulation of chemoresistance is autophagy. Hence, we studied the literatures on chemoresistance mechanisms, the miRNAs’ role in cancer, and the miRNAs’ role in chemoresistance by modulating autophagy. Graphical Abstract
      PubDate: 2020-12-01
       
  • MSC encapsulation in alginate microcapsules prolongs survival after
           intra-articular injection, a longitudinal in vivo cell and bead integrity
           tracking study
    • Abstract: Abstract Mesenchymal stem cells (MSC) are promising candidates for use as a biological therapeutic. Since locally injected MSC disappear within a few weeks, we hypothesize that efficacy of MSC can be enhanced by prolonging their presence. Previously, encapsulation in alginate was suggested as a suitable approach for this purpose. We found no differences between the two alginate types, alginate high in mannuronic acid (High M) and alginate high in guluronic acid (High G), regarding MSC viability, MSC immunomodulatory capability, or retention of capsule integrity after subcutaneous implantation in immune competent rats. High G proved to be more suitable for production of injectable beads. Firefly luciferase-expressing rat MSC were used to track MSC viability. Encapsulation in high G alginate prolonged the presence of metabolically active allogenic MSC in immune competent rats with monoiodoacetate-induced osteoarthritis for at least 8 weeks. Encapsulation of human MSC for local treatment by intra-articular injection did not significantly influence the effect on pain, synovial inflammation, or cartilage damage in this disease model. MSC encapsulation in alginate allows for an injectable approach which prolongs the presence of viable cells subcutaneously or in an osteoarthritic joint. Further fine tuning of alginate formulation and effective dosage for might be required in order to improve therapeutic efficacy depending on the target disease. Graphical Abstract
      PubDate: 2020-12-01
       
  • Single-cell sequencing reveals novel mechanisms of Aflatoxin B1-induced
           hepatotoxicity in S phase-arrested L02 cells
    • Abstract: Abstract Aflatoxin B1 (AFB1) is widely distributed in nature and is confirmed to be the most toxic of all the aflatoxins, whose predominant metabolism site is the liver. As a well-studied and vital mode of epigenetic modifications, aberrant methylation of the promoters in eukaryotic cells may cause the silence of essential genes, affecting their related transcriptional pathways and ultimately leading to the development of disease and cancers. This study investigated the mechanisms of AFB1-induced hepatotoxicity in S phase-arrested L02 cells using single-cell RNA-seq and single-cell reduced representation bisulfite sequencing (RRBS). AFB1 induced apoptosis and cell cycle S phase arrest, reduced mitochondrial membrane potential (ΔΨm), and increased reactive oxygen species (ROS) generation, as well as the DNA methylation level. Hepatotoxicity mechanism patterns induced by AFB1 in S phase-arrested L02 cells were revealed by combining single-cell RNA-seq with single-cell RRBS analysis, in which DNA methylation played a role via regulating the gonadotropin-releasing hormone receptor pathway, the Wnt signaling pathway, and the TGF-beta signaling pathway. Moreover, a novel strategy for precision toxicology exploration was obtained, including the selection of target cells, multi-group non-directional sequencing, and pathway analysis.
      PubDate: 2020-12-01
       
 
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