Subjects -> BIOLOGY (Total: 3331 journals)
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    - BIOPHYSICS (53 journals)
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    - ENTOMOLOGY (65 journals)
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BIOPHYSICS (53 journals)

Showing 1 - 53 of 53 Journals sorted alphabetically
Acta Biochimica et Biophysica Sinica     Hybrid Journal   (Followers: 6)
Advanced NanoBiomed Research     Open Access   (Followers: 2)
Annual Review of Biophysics     Full-text available via subscription   (Followers: 26)
Archives of Biochemistry and Biophysics     Hybrid Journal   (Followers: 19)
BBA Advances     Open Access  
BBA Bioenergetics     Hybrid Journal   (Followers: 6)
BBA Biomembranes     Hybrid Journal   (Followers: 12)
Biochemical and Biophysical Research Communications     Hybrid Journal   (Followers: 21)
Biochemistry and Biophysics Reports     Open Access  
Biochimica et Biophysica Acta (BBA) - General Subjects     Hybrid Journal   (Followers: 15)
Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids     Hybrid Journal   (Followers: 8)
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease     Hybrid Journal   (Followers: 14)
Biochimica et Biophysica Acta (BBA) - Molecular Cell Research     Hybrid Journal   (Followers: 13)
Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics     Hybrid Journal   (Followers: 12)
Bioinspired, Biomimetic and Nanobiomaterials     Hybrid Journal   (Followers: 2)
Biophysical Chemistry     Hybrid Journal   (Followers: 10)
Biophysical Journal     Hybrid Journal   (Followers: 50)
Biophysical Reports     Open Access  
Biophysical Reviews and Letters     Hybrid Journal   (Followers: 5)
Biophysics     Hybrid Journal   (Followers: 8)
Biophysics Reports     Open Access  
BMC Biophysics     Open Access   (Followers: 4)
Cell Biochemistry and Biophysics     Hybrid Journal   (Followers: 7)
Computational and Mathematical Biophysics     Open Access   (Followers: 1)
Current Topics in Biophysics     Open Access   (Followers: 3)
Doklady Biochemistry and Biophysics     Hybrid Journal   (Followers: 1)
European Biophysics Journal     Hybrid Journal   (Followers: 4)
Food Biophysics     Hybrid Journal   (Followers: 4)
Freshwater Biology     Hybrid Journal   (Followers: 33)
GSTF Journal of BioSciences     Open Access   (Followers: 2)
IEEE Life Sciences Letters     Hybrid Journal  
IEEE Nanotechnology Express     Hybrid Journal   (Followers: 18)
Indian Journal of Biochemistry and Biophysics (IJBB)     Open Access   (Followers: 2)
International Journal of Biochemistry and Biophysics     Open Access   (Followers: 1)
International Journal of Biophysics     Open Access  
Journal of Biopharmaceutical Statistics     Hybrid Journal   (Followers: 23)
Journal of Biophotonics     Hybrid Journal   (Followers: 1)
Journal of Biophysical Chemistry     Open Access   (Followers: 4)
Journal of Biophysics and Structural Biology     Open Access   (Followers: 2)
Journal of Medicine, Physiology and Biophysics     Open Access   (Followers: 5)
Journal of Physical Chemistry & Biophysics     Open Access   (Followers: 3)
Membranes and Membrane Technologies     Full-text available via subscription   (Followers: 2)
Nanomedicine Research Journal     Open Access  
Nanomedicine: Nanotechnology, Biology and Medicine     Hybrid Journal   (Followers: 7)
Natural Products and Bioprospecting     Open Access   (Followers: 2)
Nature Communications     Open Access   (Followers: 433)
PMC Biophysics     Open Access  
Progress in Biophysics and Molecular Biology     Hybrid Journal   (Followers: 1)
Progress in Physical Geography     Hybrid Journal   (Followers: 11)
Quarterly Reviews of Biophysics     Hybrid Journal   (Followers: 3)
Radiation and Environmental Biophysics     Hybrid Journal   (Followers: 3)
Research & Reviews : A Journal of Life Sciences     Open Access  
Statistics in Biopharmaceutical Research     Full-text available via subscription   (Followers: 16)
Similar Journals
Journal Cover
Acta Biochimica et Biophysica Sinica
Journal Prestige (SJR): 0.79
Citation Impact (citeScore): 2
Number of Followers: 6  
 
  Hybrid Journal Hybrid journal (It can contain Open Access articles)
ISSN (Print) 1672-9145 - ISSN (Online) 1745-7270
Published by Oxford University Press Homepage  [416 journals]
  • Roles of NPAS2 in circadian rhythm and disease

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      Authors: Peng L; Bai G, Pang Y.
      Pages: 1257 - 1265
      Abstract: AbstractNPAS2, a circadian rhythm gene encoding the neuronal PAS domain protein 2 (NPAS2), has received widespread attention because of its complex functions in cells and diverse roles in disease progression, especially tumorigenesis. NPAS2 binds with DNA at E-box sequences and forms heterodimers with another circadian protein, brain and muscle ARNT-like protein 1 (BMAL1). Nucleotide variations of the NPAS2 gene have been shown to influence the overall survival and risk of death of cancer patients, and differential expression of NPAS2 has been linked to patient outcomes in breast cancer, lung cancer, non-Hodgkin’s lymphoma, and other diseases. Here, we review the latest advances in our understanding of NPAS2 with the aim of drawing attention to its potential clinical applications and prospects.
      PubDate: Fri, 20 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab105
      Issue No: Vol. 53, No. 10 (2021)
       
  • Betulinic acid promotes the osteogenic differentiation of human
           periodontal ligament stem cells by upregulating EGR1

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      Authors: Li C; Qi Y, Zhou Q, et al.
      Pages: 1266 - 1276
      Abstract: AbstractPeriodontitis is one of the most common chronic inflammations of the oral cavity, which eventually leads to tooth loss. Betulinic acid (BetA) is an organic acid that has anti-inflammatory effects and is derived from fruits and plants, but its effect on the osteogenic differentiation of human periodontal ligament stem cells (hPDLSCs) is still unclear. This study aimed to explore the effect of BetA on the osteogenic differentiation of hPDLSCs and its mechanism. Our results revealed that BetA not only promoted the viability of hPDLSCs but also induced their osteogenic differentiation in a dose-dependent manner. In addition, RNA sequencing was used to screen the differentially expressed genes (DEGs) after hPDLSCs were treated with BetA, and 127 upregulated and 138 downregulated genes were identified. Gene Ontology enrichment analysis showed that DEGs were mainly involved in the response to lithium ions and the positive regulation of macrophage-derived foam cell differentiation. The Kyoto Encyclopedia of Genes and Genomes analysis results revealed that DEGs were enriched in the nuclear factor-κB and interleukin-17 signaling pathways. More importantly, we confirmed that early growth response gene 1 (EGR1), one of the three DEGs involved in bone formation, significantly promoted the expression of osteogenic markers and the mineralization of hPDLSCs. Knockdown of EGR1 obviously limited the effect of BetA on the osteogenic differentiation of hPDLSCs. In conclusion, BetA promoted the osteogenic differentiation of hPDLSCs through upregulating EGR1, and BetA might be a promising candidate in the clinical application of periodontal tissue regeneration.
      PubDate: Mon, 13 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab111
      Issue No: Vol. 53, No. 10 (2021)
       
  • Small-molecule inhibitor LF3 restrains the development of pulmonary
           hypertension through the Wnt/β-catenin pathway

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      Authors: Lei Y; Yang Q, Nie Y, et al.
      Pages: 1277 - 1289
      Abstract: AbstractPulmonary hypertension (PH) associated with congenital heart disease is a progressive hemodynamic disease that can lead to increased pulmonary vascular resistance, vascular remodeling, and even right heart failure and death. LF3 is a novel inhibitor of the reporter gene activity of β-catenin/TCF4 interaction in the Wnt/β-catenin signal pathway. However, whether this action of LF3 can prevent PH development remains unclear. In this study, we investigated the therapeutic effect of LF3 in rat primary pulmonary artery smooth muscle cells (PASMCs) of the PH model. We found that LF3 inhibited the decrease in pulmonary artery acceleration time and ejection time by ultra-high-resolution ultrasound imaging and blocked the increase of pulmonary artery systolic pressure by using the BL420 biological function experimental system and right ventricular hypertrophy index by the electronic scales. Simultaneously, it prevented the increase of α-smooth muscle actin and fibronectin and the decrease of elastin in pulmonary arteries of rats in the PH group, as revealed by an immunohistochemical analysis. Moreover, cell proliferation and migration assays showed that LF3 significantly reduced the proliferation and migration of PASMCs. Western blotting and quantitative real-time polymerase chain reaction analyses revealed that LF3 suppressed the expression of proliferating cell nuclear antigens and Bcl-2 and increased the expression of Bax but did not alter the expressions of β-catenin and TCF4. Taken together, LF3 can reduce the migration and proliferation of PASMCs and induce their apoptosis to prevent the development of PH. It would be worthwhile to explore the potential use of LF3 in the treatment of PH.
      PubDate: Thu, 19 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab103
      Issue No: Vol. 53, No. 10 (2021)
       
  • Blockade of T helper 17 cell function ameliorates recurrent Clostridioides
           difficile infection in mice

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      Authors: Wang S; Deng W, Li F, et al.
      Pages: 1290 - 1299
      Abstract: AbstractClostridioides difficile infection (CDI) is a common infection of the gastrointestinal tract. Typically, 20%–30% of CDI patients experience recurrent C.difficile infection (RCDI). Although the role of Th17 in infectious and inflammatory diseases including CDI has gained attention, reports on the correlation between Th17 and RCDI are scarce. In this study, CDI and RCDI mice models were challenged with C. difficile. Serum lactic acid dehydrogenase, inflammatory factor levels, reverse transcriptase-polymerase chain reaction, western blot analysis, hematoxylin and eosin staining, immunohistochemistry, flow cytometry analysis, and enzyme-linked immunosorbent assay were performed on the CDI, RCDI, and control group mice. The results showed more serious clinical manifestations in the RCDI group compared with those in the CDI group. More severe gut barrier disruption and higher degree of microbiota translocation were observed in the RCDI group compared with those in the CDI group. Moreover, extremely severe apoptosis was observed in HCT-116 cells incubated with the serum from RCDI mice model. In addition, higher levels of Th17 and IL-17 were detected in the blood or serum from the RCDI mouse model. Treatment with RORγt small molecule inhibitor SR1001 increased the expression of occludin, decreased the apoptotic rate of HCT-116 cells, and decreased the concentrations of Th17 and IL-17. Concisely, Th17 and IL-17 are potential indicators of RCDI and may serve as therapeutic targets for RCDI treatment. This study lays the foundation for future research on RCDI diagnosis and treatment.
      PubDate: Wed, 11 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab107
      Issue No: Vol. 53, No. 10 (2021)
       
  • Bi-allelic mutations in DNAH7 cause asthenozoospermia by impairing the
           integrality of axoneme structure

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      Authors: Wei X; Sha Y, Wei Z, et al.
      Pages: 1300 - 1309
      Abstract: AbstractAsthenozoospermia is the most common cause of male infertility. Dynein protein arms play a crucial role in the motility of both the cilia and flagella, and defects in these proteins generally impair the axoneme structure and cause primary ciliary dyskinesia. But relatively little is known about the influence of dynein protein arm defects on sperm flagella function. Here, we recruited 85 infertile patients with idiopathic asthenozoospermia and identified bi-allelic mutations in DNAH7 (NM_018897.3) from three patients using whole-exome sequencing. These variants are rare, highly pathogenic, and very conserved. The spermatozoa from the patients with DNAH7 bi-allelic mutations showed specific losses in the inner dynein arms. The expression of DNAH7 in the spermatozoa from the DNAH7-defective patients was significantly decreased, but these patients were able to have their children via intra-cytoplasmic sperm injection treatment. Our study is the first to demonstrate that bi-allelic mutations in DNAH7 may impair the integrality of axoneme structure, affect sperm motility, and cause asthenozoospermia in humans. These findings may extend the spectrum of etiological genes and provide new clues for the diagnosis and treatment of patients with asthenozoospermia.
      PubDate: Fri, 03 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab113
      Issue No: Vol. 53, No. 10 (2021)
       
  • Floralozone protects endothelial function in atherosclerosis by
           ameliorating NHE1

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      Authors: Huang N; Qiu Y, Liu Y, et al.
      Pages: 1310 - 1320
      Abstract: AbstractEndothelial dysfunction is the pathological basis of atherosclerosis. Incomplete understanding of endothelial dysfunction etiology has impeded drug development for this devastating disease despite the currently available therapies. Floralozone, an aroma flavor, specifically exists in rabbit ear grass. Recently, floralozone has been demonstrated to inhibit atherosclerosis, but the underlying mechanisms are undefined. The present study was undertaken to explore whether floralozone pharmacologically targets endothelial dysfunction and therefore exerts therapeutic effects on atherosclerosis. The Na+/H+ exchanger 1 (NHE1), a channel protein, plays a vital role in atherosclerosis. Whether NHE1 is involved in the therapeutic effects of floralozone on endothelial dysfunction has yet to be further answered. By performing oil red staining and hematoxylin–eosin staining, vascular functional study, and oxidative stress monitoring, we found that floralozone not only reduced the size of carotid atherosclerotic plaque but also prevented endothelial dysfunction in atherosclerotic rats. NHE1 expression was upregulated in the inner membrane of carotid arteries and H2O2-induced primary rat aortic endothelial cells. Inspiringly, floralozone prevented the upregulation of NHE1 in vivo and in vitro. Notably, the administration of NHE1 activator LiCl significantly weakened the protective effect of floralozone on endothelial dysfunction in vivo and in vitro. Our study demonstrated that floralozone exerted its protective effect on endothelial dysfunction in atherosclerosis by ameliorating NHE1. NHE1 maybe a drug target for the treatment of atherosclerosis, and floralozone may be an effective drug to meet the urgent needs of atherosclerosis patients by dampening NHE1.
      PubDate: Thu, 19 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab109
      Issue No: Vol. 53, No. 10 (2021)
       
  • ABL1 and Cofilin1 promote T-cell acute lymphoblastic leukemia cell
           migration

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      Authors: Luo J; Zheng H, Wang S, et al.
      Pages: 1321 - 1332
      Abstract: AbstractThe fusion gene of ABL1 is closely related to tumor proliferation, invasion, and migration. It has been reported recently that ABL1 itself is required for T-cell acute lymphoblastic leukemia (T-ALL) cell migration induced by CXCL12. Further experiments revealed that ABL1 inhibitor Nilotinib inhibited leukemia cell migration induced by CXCL12, indicating the possible application of Nilotinib in T-ALL leukemia treatment. However, the interacting proteins of ABL1 and the specific mechanisms of their involvement in this process need further investigation. In the present study, ABL1 interacting proteins were characterized and their roles in the process of leukemia cell migration induced by CXCL12 were investigated. Co-immunoprecipitation in combination with mass spectrometry analysis identified 333 proteins that interact with ABL1, including Cofilin1. Gene ontology analysis revealed that many of them were enriched in the intracellular organelle or cytoplasm, including nucleic acid binding components, transfectors, or co-transfectors. Kyoto Encyclopedia of Genes and Genomes analysis showed that the top three enriched pathways were translation, glycan biosynthesis, and metabolism, together with human diseases. ABL1 and Cofilin1 were in the same complex. Cofilin1 binds the SH3 domain of ABL1 directly; however, ABL1 is not required for the phosphorylation of Cofilin1. Molecular docking analysis shows that ABL1 interacts with Cofilin1 mainly through hydrogen bonds and ionic interaction between amino acid residues. The mobility of leukemic cells was significantly decreased by Cofilin1 siRNA. These results demonstrate that Cofilin1 is a novel ABL1 binding partner. Furthermore, Cofilin1 participates in the migration of leukemia cells induced by CXCL12. These data indicate that ABL1 and Cofilin1 are possible targets for T-ALL treatment.
      PubDate: Sat, 11 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab117
      Issue No: Vol. 53, No. 10 (2021)
       
  • Melatonin regulates proliferation and apoptosis of endometrial stromal
           cells via MT1

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      Authors: Cui L; Xu F, Jiang Z, et al.
      Pages: 1333 - 1341
      Abstract: AbstractEndometrial dysfunction is an important factor for implantation failure. The function of the endometrium is regulated by multiple factors like sex hormones and circadian rhythms. Endometrial stromal cells (ESCs) are a major cellular component in the endometrium, which is essential for proper physiological activities of the endometrium and the establishment of pregnancy. Melatonin, as a circadian-controlled hormone, plays beneficial roles in the regulation of reproductive processes. MT1, a melatonin receptor, can regulate cell proliferation and apoptosis. Whether melatonin-MT1 signal affects biological function of ESCs remains unknown. Here, we showed that MT1 was expressed in human ESCs (hESCs), which could be regulated by estrogen and progesterone. MT1 knockdown inhibited proliferative activity and promoted apoptosis of hESCs by activating caspase-3 and upregulating the Bax/Bcl2 ratio. Melatonin could reverse the effect of MT1 knockdown on proliferative activity and apoptosis of hESCs. Melatonin could promote proliferative activity of hESCs via the JNK/P38 signal pathway and repress the apoptosis of hESCs via the JNK signal pathway. Moreover, in vivo experiments showed that MT1 expression was decreased in endometrial cells from mice with disrupted circadian rhythm, accompanied by increased apoptosis and suppressed proliferative activity, which could be alleviated by administration of melatonin. These results showed the regulatory effect of melatonin-MT1 signal on biological behaviors of ESCs, which might provide a novel therapeutic strategy for endometrial dysfunction induced by disrupted circadian rhythm.
      PubDate: Tue, 03 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab108
      Issue No: Vol. 53, No. 10 (2021)
       
  • Protective mechanisms of Agrimonia pilosa Ledeb in dextran sodium
           sulfate-induced colitis as determined by a network pharmacology approach

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      Authors: Li C; Wang M, Sui J, et al.
      Pages: 1342 - 1353
      Abstract: AbstractPrevious studies reported that Agrimonia pilosa (AP) Ledeb possessed diverse biological activities, including anti-inflammatory, antioxidant, and anti-tumor activities. However, the effect of AP on ulcerative colitis (UC) remains unclear. In this study, we investigated the therapeutic effect and mechanisms of AP on dextran sodium sulfate (DSS)-induced colitis. The potential constituents of AP were investigated by ultra-high-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC-Q-TOF/MS). A total of 13 compounds were recognized by UPLC-Q-TOF/MS chromatogram. Furthermore, a network pharmacology approach revealed that there are 297 candidate targets of UC and 549 common targets for the 13 active ingredients of AP. GO enrichment and KEGG pathway analysis indicated that AP might have a protective effect on UC through the nuclear factor κB (NF-κB) and nucleotide-binding oligomerization domain (NOD)-like receptor signaling pathways. Subsequent experimental validation in a DSS-induced colitis model revealed that AP alleviated the severity of DSS-induced colitis, reduced the production of proinflammatory factors, and protected against the loss of intestinal integrity. Moreover, AP inhibited the phosphorylation of NF-κB p65 and the activation of the NLRP3 inflammasome. In conclusion, AP ameliorated DSS-induced colitis through suppressing the activation of the NLRP3 inflammasome and NF-κB signaling pathways.
      PubDate: Wed, 15 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab116
      Issue No: Vol. 53, No. 10 (2021)
       
  • Decreased dynamin-related protein 1-related mitophagy induces myocardial
           apoptosis in the aging heart

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      Authors: Wei X; Wu Y, Wang W, et al.
      Pages: 1354 - 1366
      Abstract: AbstractAn increase in cardiomyocyte apoptosis is the main contributor to the observed high morbidity of cardiac disease during aging. Mitochondria play important roles in cardiac apoptosis, and dynamin-related protein 1 (Drp1) is the critical factor that participates in mitochondrial fission and induces mitophagy to maintain mitochondria quality. However, whether Drp1 is involved in the increase of apoptosis in aging heart remains unclear. The purpose of this study was to determine whether Drp1 participates in inducing the apoptosis through regulating mitophagy in aging myocardium. To explore the effect of mitophagy and apoptosis in aging heart, we detected the expression of COX IV and the co-localization of COX IV and LC3 II, which reflect mitophagy, and measured adenosine triphosphate and reactive oxygen species contents, which reflect mitochondrial injury. Cell apoptosis was detected by measuring the activity of caspase-3 and the expression of cleaved caspase-3 and further confirmed by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay. The results showed an increase in apoptosis and a decrease in mitophagy in aging cardiomyocytes, and apoptosis was ameliorated after the induction of mitophagy by carbonyl cyanide m-chlorophenyl hydrazone (a mitophagy activator) in D-galactose (D-gal)-induced senescence H9c2 cells. To clarify the role of Drp1 in apoptosis, we knocked down Drp1 by transfecting si-Drp1, or overexpressed Drp1 in senescent cells, and then detected mitophagy, mitochondrial injury, and apoptosis. The data showed that downregulated Drp1 induces mitochondrial damage and apoptosis. In addition, to explore the regulatory relationship between Drp1 and phosphatase and tensin homologue (PTEN)-induced putative kinase 1 (PINK1)/Parkin-mediated mitophagy, we detected the expressions of PINK1 and Parkin after the overexpression of Drp1 in the D-gal group cells and found that Drp1-mediated mitophagy inhibited the PINK1/Parkin pathway in senescent cells. Our results demonstrated that insufficient Drp1 induces cardiomyocyte apoptosis by inhibiting mitophagy, and Drp1 affects the PINK1/Parkin pathway of mitophagy in the aging heart.
      PubDate: Fri, 17 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab112
      Issue No: Vol. 53, No. 10 (2021)
       
  • Circulating miR-221/222 reduces CD4+ T cells by inhibiting CD4 expression
           in colorectal cancer

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      Authors: Hu J; Zhang J, Yu M, et al.
      Pages: 1367 - 1376
      Abstract: AbstractMany patients with cancers have low levels of CD4+ in their peripheral blood. However, the molecular mechanism is still unclear. Here, we found that the blood levels of miR-221 and miR-222 were dramatically increased in patients with colorectal cancer (CRC), and both circulating miR-211 and miR-222 served as sensitive diagnostic markers with an area under the curve of 0.8790 and 0.9148, respectively. Transfection of either miR-221 or miR-222 resulted in the reduction of the surface CD4 antigen level but not the surface CD8 antigen level. The luciferase reporter assay showed that miR-221/222 directly regulated CD4 expression in human primary T cells. These data showed that miR-221/222 levels were upregulated in the blood of patients with CRC and that the expression of CD4 in human primary T cells was inhibited by miR-221/222. These findings provide a novel strategy for modulating the number of CD4+ T cells in the blood and further adjusting the microenvironment suitable for immunotherapy.
      PubDate: Fri, 06 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab106
      Issue No: Vol. 53, No. 10 (2021)
       
  • Inhibition of the lncRNA DANCR attenuates cardiomyocyte injury induced by
           oxygen-glucose deprivation via the miR-19a-3p/MAPK1 axis

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      Authors: Ruan Y; Li H, Cao X, et al.
      Pages: 1377 - 1386
      Abstract: AbstractLong noncoding RNAs (lncRNAs) have been considered as crucial regulators of acute myocardial infarction (AMI). In this study, to analyze the effect of differentiation antagonizing nonprotein coding RNA (DANCR) of lncRNA on cardiomyocyte damage in AMI, cardiomyocyte injury was induced by oxygen-glucose deprivation (OGD). Cell counting kit-8 (CCK-8) assay and flow cytometry were used to assess cell viability and apoptosis, respectively. Quantitative real-time PCR was used to measure the expression levels of DANCR and miR-19a-3p. Bioinformatics analysis and luciferase gene reporter assay were utilized to explore the relationship among DANCR, miR-19a-3p, and mitogen-activated protein kinase 1 (MAPK1). CCK-8 and TUNEL assays were used to explore the effects of DANCR alone or plus miR-19a-3p on the viability and apoptosis of OGD/R-exposed HL-1 cells. Western blot analysis was used to detect changes in the MAPK1/ERK1/2 pathway in HL-1 cells. We found that DANCR expression and miR-19a-3p level are negatively correlated as DANCR expression is increased, while miR-19a-3p level is decreased in AMI patients’ serum and OGD/R-exposed HL-1 cells. DANCR knockdown increased miR-19a-3p level, and miR-19a-3p inhibition increased DANCR expression. Moreover, DANCR directly binds to miR-19a-3p. DANCR knockdown reduced viability but induced apoptosis in OGD/R-exposed HL-1 cells, while miR-19a-3p inhibition weakens these effects. Furthermore, MAPK1 is a target of miR-19a-3p. miR-19a-3p overexpression decreases MAPK1 and ERK1/2 in HL-1 cells, while miR-19a-3p inhibition increases MAPK1 and ERK1/2 in HL-1 cells. Moreover, DANCR knockdown reduces myocardium apoptosis in mice with the left anterior descending artery ligated. DANCR knockdown effectively restores myocardial cell apoptosis by regulating the miR-19a-3p/MAPK1/ERK1/2 axis.
      PubDate: Mon, 13 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab110
      Issue No: Vol. 53, No. 10 (2021)
       
  • Targeting GRP78 enhances the sensitivity of HOS osteosarcoma cells to
           pyropheophorbide-α methyl ester-mediated photodynamic therapy via the
           Wnt/β-catenin signaling pathway

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      Authors: Zuo Q; Ou Y, Zhong S, et al.
      Pages: 1387 - 1397
      Abstract: AbstractPhotodynamic therapy (PDT), which is a new method for treating tumors, has been used in the treatment of cancer. In-depth research has shown that PDT cannot completely kill tumor cells, indicating that tumor cells are resistant to PDT. Glucose regulatory protein 78 (GRP78), which is a key regulator of endoplasmic reticulum stress, has been confirmed to be related to tumor resistance and recurrence, but there are relatively few studies on the further mechanism of GRP78 in PDT. Our experiment aimed to observe the role of GRP78 in HOS human osteosarcoma cells treated with pyropheophorbide-α methyl ester-mediated photodynamic therapy (MPPα-PDT) and to explore the possible mechanism by which the silencing of GRP78 expression enhances the sensitivity of HOS osteosarcoma cells to MPPα-PDT. HOS osteosarcoma cells were transfected with siRNA-GRP78. Apoptosis and reactive oxygen species (ROS) levels were detected by Hoechst staining and flow cytometry, cell viability was detected by Cell Counting Kit-8 assay, GRP78 protein fluorescence intensity was detected by immunofluorescence, and apoptosis-related proteins, cell proliferation-related proteins, and Wnt pathway-related proteins were detected by western blot. The results showed that MPPα-PDT can induce HOS cell apoptosis and increase GRP78 expression. After successful siRNA-GRP78 transfection, HOS cell proliferation was decreased, and apoptosis-related proteins expressions was increased, Wnt/β-catenin-related proteins expressions was decreased, and ROS levels was increased. In summary, siRNA-GRP78 enhances the sensitivity of HOS cells to MPPα-PDT, the mechanism may be related to inhibiting Wnt pathway activation and increasing ROS levels.
      PubDate: Wed, 08 Sep 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab115
      Issue No: Vol. 53, No. 10 (2021)
       
  • Inhibition of miR-144-3p exacerbates non-small cell lung cancer
           progression by targeting CEP55

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      Authors: Li M; Liu Y, Jiang X, et al.
      Pages: 1398 - 1407
      Abstract: AbstractIncreasing evidence has indicated that microRNA dysregulation is closely related to the occurrence and development of cancers. Herein, we investigated the relationship between miR-144-3p and CEP55 expression. We then evaluated the association between miR-144-3p and CEP55 expression and proliferation, invasion and apoptosis of non-small cell lung cancer (NSCLC) cells. Real-time quantitative PCR results revealed that CEP55 was over-expressed whereas miR-144-3p was under-expressed in NSCLC tissues. CCK-8 assay, wound healing assay, and flow cytometry further revealed that overexpression of miR-144-3p significantly inhibited proliferation and migration, but promoted apoptosis of A549 cells. Conversely, inhibition of miR-144-3p promoted proliferation and migration but suppressed apoptosis of H460 cells. Dual-luciferase reporter assay revealed that miR-144-3p modulated malignant properties of cancer cells by targeting CEP55. Overexpression of CEP55 partially blocked the inhibitory effect of miR-144-3p on proliferation and migration of A549 cells and induced apoptosis of A549 cells. CEP55 knockdown modulated the increase in proliferation and migration and the decrease in apoptosis of H460 cells following miR-144-3p inhibition. These findings demonstrated that miR-144-3p suppresses NSCLC development by inhibiting CEP55 expression.
      PubDate: Thu, 26 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab118
      Issue No: Vol. 53, No. 10 (2021)
       
  • Development of a double antibodies sandwich ELISA for the detection of
           avian leukosis virus subgroup J based on monoclonal antibodies against
           gp85

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      Authors: Cao L; Zhao P, Ding H, et al.
      Pages: 1408 - 1411
      Abstract: 20160204020NY20200403041SF
      PubDate: Tue, 31 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab114
      Issue No: Vol. 53, No. 10 (2021)
       
  • A direct circular dichroic assay for quantitative determination of peptide
           enantiomers

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      Authors: Yang J; Zhong S, Chen X, et al.
      Pages: 1412 - 1415
      Abstract: National Natural Science Foundation of China10.13039/50110000180931900023National Natural Science Foundation of China10.13039/50110000180931971535National Natural Science Foundation of China10.13039/50110000180932000004National Natural Science Foundation of China10.13039/501100001809U1706207National Key R&D Program of China2018YFC0310704National Key R&D Program of China2018YFC1406504National Key R&D Program of China2018YFC1406701
      PubDate: Fri, 06 Aug 2021 00:00:00 GMT
      DOI: 10.1093/abbs/gmab104
      Issue No: Vol. 53, No. 10 (2021)
       
 
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