Subjects -> BIOLOGY (Total: 3174 journals)
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CYTOLOGY AND HISTOLOGY (32 journals)

Showing 1 - 29 of 29 Journals sorted alphabetically
Acta Histochemica     Hybrid Journal   (Followers: 3)
Annals of Cytology and Pathology     Open Access   (Followers: 1)
Applied Immunohistochemistry & Molecular Morphology     Hybrid Journal   (Followers: 16)
Cell Discovery     Open Access   (Followers: 2)
Comparative Cytogenetics     Open Access   (Followers: 1)
Current Protocols in Cytometry     Hybrid Journal  
Cytogenetic and Genome Research     Full-text available via subscription   (Followers: 2)
Cytokine     Hybrid Journal   (Followers: 6)
Cytokine & Growth Factor Reviews     Hybrid Journal   (Followers: 3)
Cytokine : X     Open Access  
Cytology and Genetics     Hybrid Journal   (Followers: 4)
Cytometry Part A     Hybrid Journal   (Followers: 3)
Cytometry Part B: Clinical Cytometry     Hybrid Journal   (Followers: 4)
Cytopathology     Hybrid Journal   (Followers: 11)
Cytoskeleton     Hybrid Journal   (Followers: 1)
Cytotechnology     Hybrid Journal   (Followers: 10)
Diagnostic Cytopathology     Hybrid Journal   (Followers: 10)
Egyptian Journal of Genetics And Cytology     Open Access  
European Journal of Histochemistry     Open Access   (Followers: 4)
Folia Cryptogamica Estonica     Open Access  
Histochemistry and Cell Biology     Hybrid Journal   (Followers: 6)
Journal of Cytology & Histology     Open Access   (Followers: 5)
Journal of Histochemistry and Cytochemistry     Hybrid Journal   (Followers: 7)
Journal of Histotechnology     Hybrid Journal   (Followers: 2)
Journal of Molecular Histology     Hybrid Journal   (Followers: 5)
Journal of the American Society of Cytopathology     Hybrid Journal   (Followers: 5)
Journal of the History of Biology     Hybrid Journal   (Followers: 5)
Single Cell Biology     Open Access  
Vegetation History and Archaeobotany     Hybrid Journal   (Followers: 4)
Similar Journals
Journal Cover
Journal of Molecular Histology
Journal Prestige (SJR): 0.981
Citation Impact (citeScore): 2
Number of Followers: 5  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1567-2387 - ISSN (Online) 1567-2379
Published by Springer-Verlag Homepage  [2469 journals]
  • Ginsenoside Rb3 attenuates skin flap ischemia-reperfusion damage by
           inhibiting STING-IRF3 signaling

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      Abstract: Abstract We investigate the protective effect of ginsenoside Rb3 on skin flap microvasculature following ischemia-reperfusion (I/R) injury and its regulatory mechanism. We used a rat model of I/R injury with the right iliolumbar artery and oxidative stress model of human dermal microvascular endothelial cells. The effects of Rb3 on skin flap tissue and endothelial cell survival, STING-IRF3 pathway activation, and endothelial cell adhesion were measured. Following reperfusion, the survival rate of rat perforator flaps in the Rb3-treated group gradually increased with increasing Rb3 concentration. The treatment also reduced the amount of STING protein, phosphorylated IRF3, and P-selectin in skin flap tissue, with this change being most obvious in microvascular endothelial cells. In vitro, activated IRF3 binds to the P-selectin promoter and induces P-selectin expression. Our results suggest that Rb3 plays a role in reducing I/R flap damage through negatively regulating STING-IRF3 activation to limit leukocyte-endothelial cell adhesion.
      PubDate: 2022-06-22
       
  • Silibinin ameliorates cisplatin-induced acute kidney injury via activating
           Nfe2l1-mediated antioxidative response to suppress the ROS/MAPK signaling
           pathway

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      Abstract: Abstract Cisplatin, a first-line chemotherapeutic agent commonly used to treat various solid tumors, induce severe adverse effects, especially nephrotoxicity, which largely limits its clinical application. However, the currently used measures to prevent nephrotoxicity are not ideal owing to the mechanisms underlying cisplatin-induced nephrotoxicity are not comprehensively understood. Herein, we examined the effects of silibinin on cisplatin-induced nephrotoxicity and found that silibinin exerted cytoprotection effects during cisplatin treatment in HEK293 cells and in a cisplatin-induced acute kidney injury (AKI) model. Mechanistically, silibinin ameliorated cisplatin-induced AKI via decreasing ROS-mediated MAPK signaling pathway activation, which was confirmed using the inhibitor N-acetylcysteine. Moreover, the protective effect of silibinin against cisplatin-induced ROS generation through the antioxidant transcription factor nuclear factor-erythroid 2-related factor 1 (Nfe2l1), rather than Nfe2l2, mediates HO1 expression. Furthermore, interference with the abundance of Nfe2l1 using siRNA or an overexpression plasmid enhanced or decreased the effect of cisplatin-induced apoptosis, respectively, in HEK293 cells. Interestingly, Nfe2l1 protein stability was more sensitive to cisplatin than that of Nfe2l2. More importantly, the mechanism that silibinin activates Nfe2l1-mediated antioxidant responses was confirmed in a cisplatin-induced AKI model. Silibinin rescued cisplatin-induced Nfe2l1 inhibition by regulating its transcription and post-translational modifications. Taken together, our results reveal a novel mechanism by which silibinin ameliorates cisplatin-induced AKI via activating Nfe2l1-mediated antioxidative response, which provides a new insights to protect patients receiving cisplatin-based cancer treatment against AKI.
      PubDate: 2022-06-21
       
  • β2-adrenergic receptor drives the metastasis and invasion of pancreatic
           ductal adenocarcinoma through activating Cdc42 signaling pathway

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      Abstract: Abstract Recent investigations indicate that β2-adrenergic receptor (β2-AR) signaling may facilitate the progression of various tumors, whose underlying mechanisms remain largely elusive. In the present study, we showed that β2-AR recruited Cdc42 in response to isoproterenol (ISO, a β-AR selective agonist) exposure in pancreatic ductal adenocarcinoma (PDAC) cells. The association of β2-AR and Cdc42 promoted the activation of Cdc42, as revealed by increased levels of Cdc42-GTP, and co-incubation with β2-AR antagonist abrogated ISO-induced activation of Cdc42. β2-AR-mediated Cdc42 activation further led to the phosphorylation of downstream PAK1, LIMK1 and Merlin. Furthermore, we showed that the activation of β2-AR/Cdc42 signaling facilitated the migration and invasion of PDAC cells. In addition, β2-AR and Cdc42 were overexpressed in PDAC specimens, compared with adjacent non-tumor tissues. High expression of β2-AR and Cdc42 were correlated with lymph node metastasis and TNM stage in PDAC patients. Finally, we showed that overexpression of β2-AR and Cdc42 were indicative of unfavorable prognosis in PDAC patients. Taken together, our findings suggested that β2-AR might facilitate Cdc42 signaling to drive the migration and invasion of PDAC cells, consequently resulting in the metastasis and dismal prognosis of PDAC. These studies highlight targeting β2-AR/Cdc42 signaling as a therapeutic strategy against PDAC.
      PubDate: 2022-06-18
       
  • JAK-STAT signaling mediates the senescence of cartilage-derived
           stem/progenitor cells

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      Abstract: Abstract Aging is a major risk factor for degenerative joint diseases, such as osteoarthritis (OA). Previous studies have confirmed the link between senescent mesenchymal stem cells (MSCs) and OA. Cartilage-derived stem/progenitor cells (CSPCs) with MSCs properties have been extracted from a variety of species. We inferred that the senescence of CSPCs may promote the development of osteoarthritis. However, the cellular and molecular mechanisms of CSPCs senescence remains unknown. In this study, we investigated the role of JAK-STAT signaling pathway in a replicative senescence model of CSPCs. We showed that the late CSPCs (> 15th passage) exhibited distinct senescent phenotypes, including increased proportion of β-gal positive senescent cells and F-actin content, as well as cell cycle arrest. In late CSPCs, the activity of JAK-STAT signaling pathway was significantly increased. Activation of JAK-STAT signaling pathway promoted cell senescence in early CSPCs (< 6th passage). Conversely, pharmacological inhibition or genetic knockdown of JAK-STAT signaling pathway attenuated cell senescence in late CSPCs. In conclusion, our results demonstrated the critical role of JAK-STAT signaling pathway in CSPCs senescence.
      PubDate: 2022-06-18
       
  • CRIF1 promotes the progression of non-small-cell lung cancer by SIRT3-
           mediated deacetylation of PYCR1

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      Abstract: Abstract Lung cancer is the cancer with the highest mortality in the world. So further exploration of the pathogenesis of lung cancer is of great significance. In this study, the specific role and related mechanism of CRIF1 in non-small cell lung cancer (NSCLC) were explored in this research. TheRT-PCR, western blot and IHC assays were used to examine the expression level of CRIF1 in NSCLC tissue, tissue adjacent to carcinoma, NSCLC cell lines and human normal lung epithelial cells. Next, colony formation assay, Alamar blue Kit and EdU assays were employed to examine the proliferation of transfected A549 and NCI-H2009 cells. Measurement of mitochondrial permeability transition pore opening, ATP production and cellular oxygen consumption were used to evaluate the mitochondrial apoptosis of transfected NSCLC cells. Enzymatic activity assays for PYCR1, western blot and flow cytometry assays were used to explore the relationship between PYCR1 and CRIF1. The subcutaneous xenograft tumor mice model was established to explore the role of CRIF1 in vivo. Collectively, results revealed that CRIF1 was upregulated in NSCLC cells and tissues (p < 0.001). CRIF1 promoted proliferation of NSCLC cells (p < 0.001). CRIF1 inhibited mitochondrial apoptosis in NSCLC cells (p < 0.05). Moreover, CRIF1 promoted PYCR1 deacetylation and increased its activity through SIRT3 (p < 0.05). Deacetylation of PYCR1 reversed the antitumor effect of CRIF1 knockdown (p < 0.05). Finally, knockdown of CRIF1 inhibited the tumor growth of NSCLC in vivo (p < 0.05).This research found that CRIF1 promoted the progression of non-small-cell lung cancer by SIRT3- mediated deacetylation of PYCR1.
      PubDate: 2022-06-18
       
  • TGF-β1 receptor blockade attenuates unilateral ureteral
           obstruction-induced renal fibrosis in C57BL/6 mice through attenuating
           Smad and MAPK pathways

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      Abstract: Abstract Renal fibrosis is characterized by accumulation of extracellular matrix components and collagen deposition. TGF-β1 acts as a master switch promoting renal fibrosis through Smad dependent and/or Smad independent pathways. Thirty-five male C57BL/6 mice were divided into five groups of seven each; sham, unilateral ureteral obstruction (UUO), UUO+galunisertib (150 and 300 mg/kg/day), galunisertib (300 mg/kg/day). The UUO markedly induced renal fibrosis and injury as indicated by renal functional loss, increased levels of collagen Iα1, fibronectin and α-SMA; it also activated both the Smad 2/3 and MAPKs pathways as indicated by increased levels of TGF-β1, p-Smad 2, p-Smad 3, p-p38, p-JNK and p-ERK. These UUO-induced changes were markedly attenuated by oral administration of galunisertib, the TGFβRI small molecule inhibitor. In conclusion, we demonstrated that TGF-β1 receptor blockade can prevent UUO-induced renal fibrosis through indirect modulation of Smad and MAPKs signaling pathways and may be useful as a therapeutic agent in treatment and/or prevention of renal fibrosis.
      PubDate: 2022-06-15
       
  • Hemophagocytic lymphohistiocytosis diagnosed by bone marrow trephine
           biopsy in living post-COVID-19 patients: case report and mini-review

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      Abstract: Abstract Hemophagocytic lymphohistiocytosis (HLH) constitutes a life-threatening inflammatory syndrome. Postmortem histological findings of bone marrow (BM) from COVID-19 patients showed histiocytosis and hemophagocytosis and supported the hypothesis that secondary HLH (sHLH) may be triggered by SARS-CoV-2 infection. However, there are a limited number of sHLH cases in which trephine has been performed in living post-COVID-19 patients. Here we present a recent case and a mini-review of sHLH diagnosed by trephine biopsy in living patients after COVID-19. An 81-year-old man with a past medical history of hypertension, diabetes, ischemic stroke, was referred to the hospital to evaluate leukocytosis, pyuria, and elevation of inflammatory markers four weeks after recovering from COVID-19. Computed tomography of the abdomen did not reveal focal signs of infection or hepatosplenomegaly. The patient received intravenous meropenem and two packed red blood cell units. Leukocytes and C-reactive protein were gradually decreased. A BM biopsy was performed and the patient was discharged on cefixime. BM smear revealed severe anemia, lymphopenia, and dysplastic morphologic findings of erythroblasts, neutrophils, and megakaryocytes. Trephine biopsy revealed hypercellular marrow dyserythropoiesis, plasmacytosis, lymphocytosis, histiocytosis, hemophagocytosis, and the absence of granulomas or carcinoma. Immunohistochemistry documented a mixed population of T lymphocytes (CD3+) and B lymphocytes (CD20+). Strong positivity for CD68 confirmed histiocytosis. CD138 κ, λ staining proved polyclonal plasmacytosis. Perl’s staining showed excess hemosiderin deposits. Based on our findings, we document sHLH in trephine BM biopsy of a living post-COVID-19 patient and persistent leukocytosis, underscoring the diagnostic value of trephine biopsy in preventing life-threatening conditions such as COVID-19.
      PubDate: 2022-06-14
       
  • Inhibition of osteoclastogenesis after bisphosphonate therapy
           discontinuation: an in vitro approach

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      Abstract: Abstract Osteoclasts are specialized cells that degrade and resorb bone. Bisphosphonates (BPs) are drugs with well-known capacity to inhibit the resorption of mineralized tissues. Nitrogen-containing BPs, like alendronate (ALN) and zoledronic acid (ZA), inactivate osteoclast activity mostly by alterations on the cytoskeleton architecture of the cell. In this study, we used an in vitro model to test the hypothesis that bisphosphonates may have inhibitory effects on the osteoclastogenesis and osteoclast activity after the therapy was discontinued. Primary osteoclasts were generated from mouse bone marrow in media supplemented with 1,25-dihydroxyvitamin D3 and cultivated over bones pre-treated with ALN and ZA. The pre-saturation of the bone slices with bisphosphonates did not affect cell viability. We found, however, that by disrupting the gene expression of RANKL and OPG the osteoclastogenesis and resorption activity of osteoclasts was significantly disturbed. These inhibitory effects were confirmed by scanning electron microscopy resorption assay, assessment of osteoclast ultrastructure, and by gene expression analysis of TRAP and Cathepsin K. In conclusion, ALN and ZA adhered to the bone matrix reduced the osteoclast activity in vitro.
      PubDate: 2022-06-14
       
  • Immunohistochemical visualisation of the enteric nervous system
           architecture in the germ-free piglets

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      Abstract: Abstract The enteric nervous system (ENS), considered as separate branch of the autonomic nervous system, is located throughout the length of the gastrointestinal tract as a series of interconnected ganglionic plexuses. Recently, the ENS is getting more in the focus of gastrointestinal research. For years, the main interest and research was aimed to the enteric neurons and their functional properties in normal conditions, less attention has been paid to the germ-free animals. Germ-free (GF) piglets have clear microbiological background and are reared in sterile environment. GF piglets are regarded as clinically relevant models for studying of human diseases, as these piglets’ manifest similar clinical symptoms to humans. In this study we briefly summarised the main characteristics in immunohistochemical distribution of ENS elements in the wall of jejunum and colon of germ-free piglets.
      PubDate: 2022-06-11
       
  • IL-6 promotes low concentration of RANKL-induced osteoclastic
           differentiation by mouse BMMs through trans-signaling pathway

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      Abstract: Abstract The exact role of IL-6 in inflammatory osteoclast formation is still under debate. Our previous study demonstrated that IL-6 in the combination of sIL-6R significantly promoted low level of RANKL-induced osteoclast differentiation which was not affected by IL-6 alone. However, the precise molecular mechanisms underlying the regulation of sIL-6R-induced trans-signaling on osteoclast differentiation remains to be elucidated. Mouse bone marrow‑derived monocytes (BMMs) were isolated and cultured with RANKL and IL-6/sIL-6R in the presence or absence of sgp130. TRAP staining and pit formation assay were used to visualize multinucleated giant osteoclasts and evaluate their bone resorption ability. Western blot and real time-PCR were applied to determine the activations of IL-6 signaling pathway and osteoclastogenesis- associated signaling pathways. The results showed that sIL-6R activation of IL-6 trans-signaling enhanced IL-6 signaling cascades and promoted low concentration of RANKL-induced osteoclasts formation and bone resorption by mouse BMMs. Furthermore, blocking IL-6 trans-signaling with sgp130 abrogated this promotive effect by suppressing NF-κB and JNK signaling pathways. In conclusion, sIL-6R-mediated trans-signaling pathway plays a decisive role in promotion of low level of RANKL-induced osteoclastic differentiation by IL-6/sIL-6R and targeting the IL-6 trans-signaling pathway may represent a potential strategy for inflammatory diseases with pathological bone resorption.
      PubDate: 2022-06-06
       
  • Distribution of interstitial cells of Cajal in the Esophagus and change in
           distribution after thoracic trauma

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      Abstract: Abstract Interstitial cells of Cajal (ICCs) function as pacemaker cells in the gastrointestinal tract. Acute thoracic trauma is a common and lethal cause of death due to physical trauma caused by traffic accidents. This study aimed to explore the distribution of esophageal ICCs and distribution changes observed after acute thoracic trauma. Thirty rabbits were randomly divided into a control group and two study groups. The control group animals underwent an esophagectomy. All animals in the study groups underwent right chest puncture using the Hopkinson bar technique. The study groups were subjected to esophagectomy 24 and 72 h after chest puncture. Distribution, morphology, and density of esophageal ICCs were detected using transmission electron microscopy, toluidine blue staining, and immunohistochemistry. Apoptosis of esophageal ICCs was evaluated using the terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling assay. Western blotting and reverse transcription polymerase chain reaction were used to detect changes in the SCF/c-kit signaling pathway. Esophageal ICCs distribution and SCF/c-kit signal pathway decreased from the upper part to the lower part in both physiological state and after thoracic trauma. In contrast, death of ICCs increased from the upper part to the lower part, both in physiological and injured state (P < 0.05). After thoracic trauma, increased ICCs and decreased death of ICCs in all parts of the esophagus (P < 0.05) were observed. The observed distribution and changes in esophageal ICCs would have an impact on motility and motility disorders of the esophagus.
      PubDate: 2022-06-04
       
  • Effects of PHD and HSP90 on erythropoietin production in yak (Bos
           grunniens) renal interstitial fibroblast-like cells under hypoxia

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      Abstract: Abstract Erythropoietin (EPO), a central protein of erythropoiesis, plays an important role during hypoxia adaptation and is regulated by hypoxia-inducible factor (HIF). However, there is no report on EPO-producing cells and their regulatory mechanisms in yak (Bos grunniens). To understand EPO production and regulation of yak, kidneys from different age of yak were collected and expression of EPO, hypoxia-inducible factor 1 alpha (HIF-1α), and hypoxia-inducible factor 2 alpha (HIF-2α) were detected. Then renal tubule epithelial cells (RTECs) and peritubular interstitial fibroblast-like (RIFs) cells were isolated and cultured to determine their EPO production abilities. Subsequently, the cells were treated with dimethyloxalylglycine (DMOG) and Geldanamycin (GA), which are inhibitors of prolyl-4-hydroxylase domain (PHD) and heat shock protein 90 (HSP90) respectively, and siRNAs of HIF-1α and HIF-2α to explore their effect on EPO production and regulation. The results showed that expressions of EPO, HIF-1α, and HIF-2α were different in the different age groups of yak. High DMOG concentration caused a corresponding increase in the levels of HIF-1α and HIF-2α in RIFs and RTECs, however, EPO levels increased in RIFs only and was not detected at any concentration in RTECs; suggesting that EPO was produced in RIFs. Upon treating RIFs with siRNAs of HIF-1α and HIF-2α, we found that EPO was regulated by PHD through HIF-2α. In addition, increasing GA concentration caused a decrease in expression of HSP90, HIF-1α, HIF-2α, and EPO in RIFs. In conclusion, these findings support our proposition that PHD regulates EPO via HIF-2α in yak RIFs, while HSP90 impelled EPO expression.
      PubDate: 2022-04-01
       
  • Glucose-6-phosphate dehydrogenase promotes the proliferation and migration
           of lung adenocarcinoma cells via the STAT3 signaling pathway

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      Abstract: Abstract Lung adenocarcinoma (LUAD) is the most common histological subtype of lung cancer, and the leading cause of cancer-related deaths worldwide. G6PD has been reported to enhance the progression of various tumors by regulating the intracellular redox state and mediating nucleic acid synthesis. However, the biological role and molecular mechanism of G6PD in LUAD remain largely unknown. In this study, we found that G6PD was significantly upregulated in LUAD specimens and cell lines, and that the high levels of G6PD expression were closely associated with a poor prognosis for LUAD patients. Moreover, we found that G6PD significantly promoted the proliferation and migration of LUAD cells in vitro, and overexpression of G6PD also play a role of facilitating tumorigenesis in in vivo experiments. Mechanistically, the STAT3 signaling pathway was significantly activated by G6PD-mediated LUAD progression. Overall, our results suggest that G6PD could serve as a novel prognostic marker and therapeutic target for treating LUAD.
      PubDate: 2022-04-01
       
  • Zkscan3 affects erythroblast development by regulating the transcriptional
           activity of GATA1 and KLF1 in mice

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      Abstract: Abstract ZKSCAN3 encodes a zinc-finger transcription factor that regulates the expression of important genes and plays a significant role in tumor development, pathogenesis, and metastasis. However, its biological functions under normal physiological conditions remain largely unknown. In our previous studies, using flow cytometry, we found that the deletion of Zkscan3 may cause abnormal erythropoiesis. In this study, we found that, in a Zkscan3 knockout mice model, the number of splenic early-stage (basophilic-erythroblasts) and late-stage (chromatophilic-erythroblasts to polychromatophilic-erythroblasts through orthochromatophilic-erythroblasts) erythroblasts increased, whereas the number of late erythroblasts in the bone marrow decreased. Moreover, the phenotype was exacerbated after treating mice with phenylhydrazine (PHZ), which causes severe hemolytic anemia. In the knockout mice treated with PHZ, the percentage of reticulocyte in the peripheral blood conspicuously increased, whereas MCHC and red blood cells decreased. Then, we performed RNA-seq and quantitative-polymerase chain reaction assay and found that the expression of GATA1 and Tiam1 in erythroblasts were upregulated, whereas KLF1 was downregulated. Luciferase assays showed that Zkscan3 inhibited the transcription of GATA1 and Tiam1 and promoted the expression of KLF1. Additionally, ChIP and CO-IP results confirmed that Zkscan3 directly interacts with GATA1 and inhibits its transcriptional activity in MEL cells. Our results demonstrate, for the first time, the significant role of Zkscan3 in physiological erythropoiesis through the interaction with GATA1, both at the DNA and protein level, and with Tiam1 and KLF1 at the DNA level.
      PubDate: 2022-04-01
       
  • Comparative microanatomical and histochemical biodistribution profiles of
           different types of mucins in the intestinal mucosa of some tetrapod
           representatives

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      Abstract: Abstract The microanatomical features of the intestinal tract mucosa layer in different species of tetrapoda vary according to the type of species, tissue, and function of the targeted cells. In the present study, we have evaluated the histological and histochemical variations of the intestinal tract in four species representing superclass tetrapoda. Bufo regularis (toad), Trachylepis quinquetaeniata (lizard), Columba livia domestica (pigeon) and Mus musculus (mouse) were used as representatives for amphibians, reptilians, avians and mammalians respectively. Histologically, the ileum’s mucosal layer of the lower tetrapods (toad and lizard) was almost similar and consists of elongated finger-like shape villi lined with simple columnar epithelium and goblet cells. Similarly, the microanatomical features in ileum of higher tetrapod representatives (pigeon and mouse) were characterized by the presence of villi lined with simple columnar epithelium and scattered goblet cells as well as intestinal glands (crypts of Lieberkühn) at the bases of the intestinal villi. In the toad rectum, the mucosal layer was similar to that of the ileum but with shorter villi and more numerous goblet cells. However, the mucosal layer of the rectum in the lizard had low numbers of absorptive columnar epithelial cells with abundant goblet basal cells. Comparatively, the pigeon’s rectal mucosa had almost a similar structure to that of ileum but in leaf-like shaped villi. Finally, the rectum of the mouse has narrow rectal pits, instead of villi, lined with goblet cells and absorptive epithelial cells. Histochemically, the ileum in the four studied tetrapod representatives showed varying biodistribution profiles of neutral, sulfated and carboxylated mucins. There are variations encountered in the intestinal brush border and goblet cells of villi in all species as well as the crypts of Lieberkühn in higher tetrapods. Also, the rectum of all tetrapod species showed weak to strong positive signals for the three types of mucins in the brush border and goblet cells of villi in all species and crypts of Lieberkühn in higher tetrapods as well. In addition, the brush border of toad’s rectum was lacking sulfated mucins and that of the lizard did not have any type of mucins. The data of this study will contribute to understand the relationship between the microanatomical features and mucins biodistribution profiles in the mucosal layer of tetrapod intestinal tract and their functions.
      PubDate: 2022-03-06
      DOI: 10.1007/s10735-022-10071-z
       
  • Silence of MLK3 alleviates lipopolysaccharide-induced lung epithelial cell
           injury via inhibiting p53-mediated ferroptosis

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      Abstract: Abstract Acute lung injury (ALI) is characterized with a high rate of morbidity and mortality. The injury and apoptosis of lung epithelial cells play crucial roles in the progression of ALI. Mixed lineage kinase 3 (MLK3) has been reported to be involved in the regulation of cellular biological functions, such as cell proliferation, apoptosis and ferroptosis. However, the effect of MLK3 exerted on ALI has not been reported. Here, LPS-stimulated MLE12 pulmonary epithelial cells were used as an in vitro model for ALI. In this research, LPS elevated the expression of MLK3 in MLE12 cells. The silence of MLK3 alleviated LPS-induced cell injury. Notably, LPS promoted ferroptosis through enhancing GSH depletion and the productions of MDA and iron, which was attenuated by MLK3 knockdown. Moreover, the silence of MLK3 inhibited p53 expression in LPS-induced cells along with a decrease in the expressions of p21 and Bax, while overexpressing p53 reversed these effects of MLK3 silence. Meanwhile, p53 overexpression reversed the positive effects of MLK3 knockdown on LPS-induced cell ferroptosis and injury. Together, our results confirmed that the silence of MLK3 alleviated LPS-induced lung epithelial cell injury by inhibiting p53-mediated ferroptosis.
      PubDate: 2022-03-05
      DOI: 10.1007/s10735-022-10064-y
       
  • Intrinsic innervation of the ovary and its variations in the rat
           senescence process

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      Abstract: Abstract Ovarian functions decrease with perimenopause. The ovary has extrinsic innervation, but the neural influence on ovarian functions and dysfunction is not well-studied. The present study aimed to biochemically and morphometrically characterize the intrinsic neurons in ovaries from young adult, middle-aged, and senescent Long Evans CII-ZV rats (3, 12, and 15 months old, respectively). Ovaries were extracted from four rats of each age group (n = 12 total), cryopreserved, and processed for immunofluorescence studies with the primary NeuN/β-tubulin and NeuN/tyrosine hydroxylase (TH) antibodies. The soma area and number of intrinsic neurons in the ovarian stroma, surrounding follicles, corpus luteum, or cyst were evaluated. The intrinsic neurons were grouped in cluster-like shapes in ovarian structures. In senescent rats, the intrinsic neurons were mainly localized in the ovarian stroma and around the cysts. The number of neurons was lower in senescent rats than in young adult rats (p < 0.05), but the soma size was larger than in young adult rats. Immunoreactivity to TH indicated the presence of noradrenergic neurons in the ovary with the same characteristics as NeuN/β-tubulin, which indicates that they are part of the same neuronal group. Taken together, the findings indicate that the intrinsic neurons may be related to the loss of ovarian functions associated with aging.
      PubDate: 2022-02-25
      DOI: 10.1007/s10735-022-10069-7
       
  • Transcriptomic analysis and biological evaluation reveals that LMO3
           regulates the osteogenic differentiation of human adipose derived stem
           cells via PI3K/Akt signaling pathway

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      Abstract: Abstract Autologous bone transplantation which is a common treatment method for bone defects needs a large quantity of bone cells. In order to develop new treatments to regenerating bone tissues, this research aimed at identifying the key genes and finding their mechanism in human adipose-derived stem cells (hADSCs) osteogenesis. GSE63754, GSE89330 and GSE72429 were downloaded to perform GO functional and KEGG pathway analyses, construct a competing endogenous RNA (ceRNA) network, construct a PPI network and identify hub genes. The expression level of LMO3 during the osteogenesis of hADSCs was examined by quantitative reverse transcription polymerase chain reaction and western blot. Lentivirus transfection was used to knock down or overexpress LMO3, which enabled us to investigate the effect of LMO3 on osteogenic differentiation of hADSCs. Wortmannin were used to identify the mechanism of the LMO3/PI3K/Akt axis in regulating osteogenic differentiation of hADSCs. Moreover, ectopic bone formation in nude mice was used to investigate the effect of LMO3 on osteogenesis in vivo. In this study, we found the expression of LMO3 was significantly upregulated during the osteogenic differentiation of hADSCs. LMO3 knockdown remarkably suppressed osteogenic differentiation of hADSCs, while LMO3 overexpression promoted osteogenic differentiation of hADSCs both in vitro and in vivo. Moreover, we discovered that the enhancing effect of LMO3 overexpression on osteogenic differentiation was related to the activation of PI3K/Akt signaling pathway. Inhibition of PI3K/Akt signaling pathway with wortmannin effectively blocked the stimulation of osteogenic differentiation induced by LMO3 overexpression. In conclusion, based on transcriptomic analysis, we identified key genes involved in regulating the osteogenic differentiation of hADSCs. In addition, we found that LMO3 might act as a positive modulator of hADSC osteogenic differentiation by mediating PI3K/Akt signaling pathway. Manipulating the expression of LMO3 and its associated pathways might contribute to advances in bone regeneration and tissue engineering.
      PubDate: 2022-02-14
      DOI: 10.1007/s10735-021-10047-5
       
  • Acetyl CoA synthase 2 potentiates ATG5-induced autophagy against neuronal
           apoptosis after subarachnoid hemorrhage

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      Abstract: Abstract ATG5-induced autophagy is triggered in the early stages after SAH, which plays a vital role in subarachnoid hemorrhage (SAH). Acyl-CoA synthetase short-chain family 2 (ACSS2) is not just involved in energy metabolism but also binds to TEFB to form a complex translocated to related autophagy genes to regulate the expression of autophagy-related genes. However, the contribution of ACSS2 to the activation of autophagy in early brain injury (EBI) after SAH has barely been discussed. The purpose of this study was to investigate the alterations of ACSS2 and its neuroprotective effects following SAH. We first evaluated the expression of ACSS2 at different time points (6, 12, 24, and 72 h after SAH) in vivo and primary cortical neurons stimulated by oxyhemoglobin (OxyHb). Subsequently, adeno-associated virus and lentivirus were used to regulate ACSS2 expression to investigate the effect of ACSS2 after SAH. The results showed that the ACSS2 level decreased significantly in the early stages of SAH and was minimized at 24 h post-SAH. After artificial intervention to overexpress ACSS2, ATG5-induced autophagy was further enhanced in EBI after SAH, and neuronal apoptosis was alleviated to protect brain injury. In addition, brain edema and neurological function scores were improved. These results suggest that ACSS2 plays an important role in the neuroprotection against EBI after SAH by increasing ATG5-induce autophagy and inhibiting apoptosis.
      PubDate: 2022-02-08
      DOI: 10.1007/s10735-022-10057-x
       
  • Isolation, culture, and identification of ceruminous gland cells

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      Abstract: Abstract External auditory canal (EAC) stenosis or atresia usually requires a skin graft to repair, but due to the lack of a graft containing functional glands, postoperative complications such as infection and eczema are common. The aim of this study was to isolate and characterize seed cells for the construction of tissue engineered EAC skin containing ceruminous gland by isolating and cultivating cells of ceruminous gland. In this study, EAC skin samples were harvested from adult goats for ceruminous gland cell isolation. Cell morphology and proliferation rates, expression of CK7, CK8, CK18, and CK19 (glandular cell specific-markers), and secretion of β-defensin-1, lysozyme, and polysaccharides were evaluated at different passages to verify the presence of ceruminous gland cells and determine whether function and proliferation potential were maintained. Ceruminous glands were successfully isolated and extracted from goat EAC skin. Furthermore, the isolated glandular cells maintained robust proliferation potential, exhibited high expression of CK7, CK8, CK18, and CK19, and vigorously secreted β-defensin-1, lysozyme, and polysaccharides in this culture system. However, expression of glandular cell specific-markers and secretory function gradually declined with increasing passage number, indicating dedifferentiation of the subcultured ceruminous gland cells after five passages. In conclusion, ceruminous glands were successfully isolated, cultured, and expanded from goat EAC skin using the serumcontaining culture system. Importantly, the isolated glandular cells retained robust proliferation potential and maintained their phenotype and function in early passages (P1–P3), indicating the method’s potential application for ceruminous gland regeneration.
      PubDate: 2022-02-03
      DOI: 10.1007/s10735-021-10040-y
       
 
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