General physiology and biophysics最新文献_第8页

LncRNA XIST promotes insulin resistance in gestational diabetes mellitus via the microRNA-181b-5p/NDRG2 axis. LncRNA XIST通过microRNA-181b-5p/NDRG2轴促进妊娠期糖尿病胰岛素抵抗。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-09-01 DOI: 10.4149/gpb_2023019

Yanli Xu, Xiaodi Kang, Huafang Liu, Hongli Jiang, Wenjing Wang

{"title":"LncRNA XIST promotes insulin resistance in gestational diabetes mellitus via the microRNA-181b-5p/NDRG2 axis.","authors":"Yanli Xu, Xiaodi Kang, Huafang Liu, Hongli Jiang, Wenjing Wang","doi":"10.4149/gpb_2023019","DOIUrl":"https://doi.org/10.4149/gpb_2023019","url":null,"abstract":"Many studies have explored the role of lncRNA X inactivation-specific transcript (XIST) in diabetes. This study was designed to unravel the regulatory mechanism of XIST on animal models of gestational diabetes mellitus (GDM) progression via the microRNA (miR)-181b-5p/N-myc downstream-regulated gene 2 (NDRG2) axis. XIST, miR-181b-5p, and NDRG2 expression levels in GDM mice were detected. The GDM mice were subjected to gain- and loss-of-function assays to examine the change of glucose metabolism indices (fasting blood glucose (FBG), fasting insulin (FINS) and homeostasis model assessment of insulin resistance (HOMA-IR)), serum oxidative stress factors (glutathione (GSH), superoxide dismutase (SOD), and malondialdehyde (MDA)), serum inflammatory factors (interleukin-1 β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α)), pathological changes of pancreatic tissues, and apoptotic cells in pancreatic islets in GDM mice. XIST and NDRG2 expression were elevated while miR-181b-5p expression was depleted in GDM mice. Down-regulated XIST or NDRG2 or up-regulated miR-181b-5p reduced the FBG level, HOMA-IR, and serum IL-1β, IL-6, and TNF-α, and MDA contents, elevated the FINS, GSH, and SOD level, mitigated pathological changes in pancreatic tissues, and decelerated apoptotic cells in pancreatic islets in GDM mice. Silenced XIST dampens insulin resistance in GDM mice via the modulation of the miR-181b-5p/NDRG2 axis.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 5","pages":"443-455"},"PeriodicalIF":1.5,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10233843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

DNMT1-induced miR-133b suppression via methylation promotes myocardial fibrosis after myocardial infarction. dnmt1通过甲基化诱导的miR-133b抑制促进心肌梗死后心肌纤维化。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-09-01 DOI: 10.4149/gpb_2023018

Songlin Zhang, Hang Xie, Yajuan Du, Boxiang Wang, Beidi Lan, Haiyan Wang

{"title":"DNMT1-induced miR-133b suppression via methylation promotes myocardial fibrosis after myocardial infarction.","authors":"Songlin Zhang, Hang Xie, Yajuan Du, Boxiang Wang, Beidi Lan, Haiyan Wang","doi":"10.4149/gpb_2023018","DOIUrl":"https://doi.org/10.4149/gpb_2023018","url":null,"abstract":"Myocardial fibrosis is an underlying cause of many cardiovascular diseases. Novel insights into the epigenetic control of myocardial fibrosis are now emerging. The current work is focused on investigating the biological role of DNA methyltransferase 1 (DNMT1) in myocardial fibrosis as well as the underlying mechanism. Our findings revealed that DNMT1 expression levels were upregulated, whereas miR-133b expression levels were decreased in a rat model of myocardial fibrosis following myocardial infarction. In vitro, the expression levels of DNMT1 increased and those of miR-133b decreased after Ang-II treatment in cardiac fibroblasts. DNMT1 knockdown inhibited Ang-II-induced cardiac myofibroblast activation, and DNMT1 overexpression increased the proliferation and collagen generation of cardiac myofibroblasts. Furthermore, DNMT1 expression levels decreased, while miR-133b expression levels increased after treatment with 5-Aza (5-Azacytidine, a known inhibitor of DNA methylation) in Ang-II-induced cardiac fibroblasts. BSP (Bisulfite sequencing PCR) results showed a marked decrease in methylation levels in the miR-133b promoter region upon overexpression of DNMT1, whereas knockdown of DNMT1 blocked increased methylation levels in the miR-133b promoter region in Ang-II-induced cardiac fibroblasts. Finally, 5-Aza treatment reduced the progression of myocardial fibrosis after myocardial infarction in rats in vivo. Collectively, our results suggest that DNMT1 mediates CTGF expression in cardiac fibroblast activation by regulating the methylation of miR-133b. The present work reveals the unique role of the DNMT1/miR-133b/CTGF axis in myocardial fibrosis, thus suggesting its great therapeutic potential in the treatment of cardiac diseases.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 5","pages":"417-429"},"PeriodicalIF":1.5,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10259505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

The morphological and functional ultrastructure of cells in pre-implantation embryos. 着床前胚胎细胞的形态和功能超微结构。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023011

Juraj Pivko, Alexander Makarevich, Lucia Olexiková, Elena Kubovičová, Peter Makovický, Linda Dujičková, Jiří Bezdíček

{"title":"The morphological and functional ultrastructure of cells in pre-implantation embryos.","authors":"Juraj Pivko, Alexander Makarevich, Lucia Olexiková, Elena Kubovičová, Peter Makovický, Linda Dujičková, Jiří Bezdíček","doi":"10.4149/gpb_2023011","DOIUrl":"https://doi.org/10.4149/gpb_2023011","url":null,"abstract":"Cells of pre-implantation embryos are equipped with many morphological and functional systems through which they can synthesize specific proteins and effectively ensure the protection of early embryonic development. Here we present evidence for the existence of these systems in morphologically normal and abnormal bovine blastocyst stage embryos in vivo at the ultrastructural and actin cytoskeleton levels. The appearance of organelles in the trophectoderm (TE) and inner cell mass (ICM) cells, responsible for their synthetic activities and their role in the development of early bovine embryos are described. We point out the importance of endocytic processes and the participation of extracellular vesicles in the formation of intercellular contacts and homeostasis of the embryo microenvironment. Several changes in the ultrastructural morphology of embryos produced by different methods (ICSI, parthenogenetic AC/DC electrical activation, IVF with separated sperm) and freezing/thawed embryos are described. We also show alterations occurred in the organelles after viral contamination of embryos with BHV-1 and BVDV viruses, and in embryos from over-conditioned cows. Recorded changes in organelles and appearance of cellular autophagic structures (vesicles, multivesicular bodies and autophagolysosomes) may negatively affect embryo metabolism and lead to the emergence of pathological processes in TE and ICM cells of preimplantation embryos.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 4","pages":"307-321"},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9820975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biomedical research brings mTBI biomarkers a step closer to the bedside - implementation in clinical practice. 生物医学研究使mTBI生物标志物在临床实践中更接近床边实施。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023013

Martina Martinikova, Robert Ruzinak, Egon Kurca, Michael Teodor Grey, Stefan Sivak

{"title":"Biomedical research brings mTBI biomarkers a step closer to the bedside - implementation in clinical practice.","authors":"Martina Martinikova, Robert Ruzinak, Egon Kurca, Michael Teodor Grey, Stefan Sivak","doi":"10.4149/gpb_2023013","DOIUrl":"https://doi.org/10.4149/gpb_2023013","url":null,"abstract":"Research in the field of TBI (traumatic brain injury) has long been focused on severe brain injury, while the number of mild injuries far overweigh severe injuries. Mild head injuries constitute up to 95% of all traumatic head injuries. The purpose of this work is to identify mTBI (mild traumatic brain injury) patients who are unlikely to benefit from CT (computed tomography) scanning. Biomarkers capable of clearly discriminating between CT-positive and CT-negative subjects are needed. Biomarkers hold the potential to document whether a concussion occurred, especially when the history is unclear and neurocognitive sequelae persist. Recently, following advances in proteomics analysis, investigators have introduced ubiquitin C-terminal hydrolase-L1 (UCH-L1) and glial fibrillary acidic protein (GFAP) as two promising brain injury biomarkers. The authors provide an update on the current knowledge of TBI biomarkers, especially protein biomarkers for neuronal cell body injury (UCH-L1) and astroglial injury (GFAP, S100B), and a focused literature review dealing with implementation of mTBI biomarkers in clinical practice.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 4","pages":"323-338"},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9820977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Correction: Chloroquine inhibits vasodilation induced by ATP-sensitive potassium channels in isolated rat aorta. 更正:氯喹抑制离体大鼠主动脉atp敏感钾通道诱导的血管舒张。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023014

Kyeong-Eon Park, Soo Hee Lee, Sung Il Bae, Yeran Hwang, Seong-Ho Ok, Dawon Kang, Seung Hyun Ahn, Gyujin Sim, Jin Kyeong Park, Ju-Tae Sohn

引用次数: 0

Targeting AMPK/eNOS pathway and mitochondria by sonlicromanol protects myocardial cells against ischemia-reperfusion injury. sonlicromanol靶向AMPK/eNOS通路和线粒体对心肌细胞缺血再灌注损伤具有保护作用。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023003

Kun Liao, Fangfei Huang, Xing Xie, Linhui Li

{"title":"Targeting AMPK/eNOS pathway and mitochondria by sonlicromanol protects myocardial cells against ischemia-reperfusion injury.","authors":"Kun Liao, Fangfei Huang, Xing Xie, Linhui Li","doi":"10.4149/gpb_2023003","DOIUrl":"https://doi.org/10.4149/gpb_2023003","url":null,"abstract":"This work evaluated the cardioprotective effects of sonlicromanol, a new mitochondrial-directed drug, on cardiac ischemia/reperfusion (I/R) injury and explored the involvement of inflammatory and oxidative responses via activation of AMPK-eNOS-mitochondrial pathway. Male Sprague-Dawley rats underwent regional I/R injury through in vivo left anterior descending (LAD) coronary artery ligation for 40 minutes followed by 24 hours of reperfusion. Pretreatment of rats with sonlicromanol considerably reduced cardiac I/R injury in a dose-dependent manner, as indicated by lower infarct size and serum creatine-kinase levels, and improved cardiac function after reperfusion. Sonlicromanol (50 mg/kg) significantly reduced TNF-α, interleukin-1β, NF-κB-p65, and 8-isoprostane levels while increased manganese-superoxide dismutase and nitric-oxide levels and expression of eNOS and AMPK protein. It significantly reduced mitochondrial membrane depolarization and reactive oxygen species (ROS) levels. However, AMPK inhibition significantly reduced sonlicromanol protective actions. Cardioprotection by sonlicromanol was achieved by moderating inflammatory and oxidative responses, and AMPK/eNOS/mitochondrial signaling is a crucial regulator of these actions.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 4","pages":"373-382"},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9813956","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

BST-1 aggravates aldosterone-induced cardiac hypertrophy via the Ca2+ /CaN/NFATc3 pathway. BST-1通过Ca2+ /CaN/NFATc3途径加重醛固酮诱导的心肌肥厚。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2022063

Yao Yuan, Lina Zhao, Hongjuan Cao, Sha Li, Chunyan Liao, Lei Fu, Xing Wang, Fuqin Huang, Weidan Zeng, Aiyue Li, Bei Zhang

{"title":"BST-1 aggravates aldosterone-induced cardiac hypertrophy via the Ca2+ /CaN/NFATc3 pathway.","authors":"Yao Yuan, Lina Zhao, Hongjuan Cao, Sha Li, Chunyan Liao, Lei Fu, Xing Wang, Fuqin Huang, Weidan Zeng, Aiyue Li, Bei Zhang","doi":"10.4149/gpb_2022063","DOIUrl":"https://doi.org/10.4149/gpb_2022063","url":null,"abstract":"BST-1 (bone marrow stromal cell antigen-1) is thought to be a key molecule involved in regulating the functional activity of cells in various tissues and organs. BST-1 can catalyze the hydrolysis of nicotinamide adenine dinucleotide (NAD+) to produce cyclic ADP ribose (cADPR), which activates the activity of intracellular Ca2+ signaling. Currently, the role of BST-1 regulation of Ca2+ signaling pathway in pathological myocardial hypertrophy is unclear. We found elevated expression of BST-1 in cardiac hypertrophy tissues of spontaneously hypertensive rats in our vivo study, subsequently; the mechanism of BST-1 action on myocardial hypertrophy was explored in vitro experiment. We used aldosterone (ALD) to induce H9C2 cellular hypertrophy. cADPR levels and intracellular Ca2+ concentrations declined and calcium-regulated neurophosphatase (CaN) activity and protein expression were decreased after BST-1 knockdown. And then activated T-cell nuclear factor (NFATc3) entry nucleus was inhibited. All of the above resulted in that H9C2 cells size was reduced by rhodamine-phalloidin staining. Thus, BST-1 may exacerbate cardiac hypertrophy by activating the Ca2+/CaN/NFATc3 pathway.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 4","pages":"349-360"},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9826359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction. 收缩。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023016

Yao Chen, Yanmei Wang, Congcong Li, Xuechang Li, Tiejun Yuan, Shuqin Yang, Xuechang Sun

引用次数: 0

Weighted gene coexpression network analysis reveals negative regulation of hypertrophic cardiomyopathy by carboxylesterase 1 and cathepsin C. 加权基因共表达网络分析显示羧酸酯酶1和组织蛋白酶C对肥厚性心肌病有负调控作用。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023009

Ye Kuang, Jia Wang, Yulin Dong, Yun Cheng, Hongyan Li, Yong Ji, Hui Gao, Xianghong Cao

{"title":"Weighted gene coexpression network analysis reveals negative regulation of hypertrophic cardiomyopathy by carboxylesterase 1 and cathepsin C.","authors":"Ye Kuang, Jia Wang, Yulin Dong, Yun Cheng, Hongyan Li, Yong Ji, Hui Gao, Xianghong Cao","doi":"10.4149/gpb_2023009","DOIUrl":"https://doi.org/10.4149/gpb_2023009","url":null,"abstract":"Hypertrophic cardiomyopathy (HCM) is a primary cardiomyopathy characterized by hypertrophic cardiomyocytes. It is one of the leading causes of sudden death in adolescents. However, the molecular mechanism of HCM is not clear. In our study, ribonucleic acid (RNA) sequence data of myocardial tissue in HCM patients were extracted from the Gene Expression Omnibus (GEO) database (GSE130036) and analyzed by weighted gene coexpression network analysis (WGCNA). A total of 31 coexpression modules were identified. The coexpression black module significantly correlated with maximum left ventricular wall thickness (Maxi LVWT). We screened the differentially expressed mRNAs between normal tissues and HCM tissues using the dplyr and tidyr packages in R3.6.2. The genes in the black module and differentially expressed genes were further intersected. We found that the expression of carboxylesterase 1 (CES1) and cathepsin C (CTSC) was downregulated in HCM tissues and negatively correlated with Maxi LVWT. We further verified the expression of CES1 and CTSC was downregulated in HCM clinical blood and negatively correlated with Maxi LVWT. Finally, we demonstrated that overexpression of CTSC and CES1 could alleviate HCM in an HCM cell model. In summary, the study suggests that CES1 and CTSC negatively regulate the development of HCM and have potential as therapeutic and diagnostic targets for HCM.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 4","pages":"361-372"},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9820978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

A diagnostic model based on gene biomarkers for Crohn's disease. 基于基因生物标志物的克罗恩病诊断模型。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-07-01 DOI: 10.4149/gpb_2023012

Shasha Wu, Lin Zeng, Jisheng Wang

{"title":"A diagnostic model based on gene biomarkers for Crohn's disease.","authors":"Shasha Wu, Lin Zeng, Jisheng Wang","doi":"10.4149/gpb_2023012","DOIUrl":"https://doi.org/10.4149/gpb_2023012","url":null,"abstract":"Crohn's disease (CD) is a segmental chronic inflammatory bowel disease, which seriously affects the patient's quality of life. The etiology of CD is not yet clear, and there is still a lack of effective treatments. Therefore, in this study, we focus on developing a useful model for early diagnosis and targeted therapy of CD. The expression datasets of CD were collected to filter differentially expressed genes (DEGs) by overlapping \"limma\" package and \"WGCNA\" package. Then, functional enrichment analysis and protein-protein interaction (PPI) network analyses were performed. Hub genes were screened with \"cytoHubba\" plug-in and filtered with LASSO and stepwise regression analyses. The logistic regression model and nomogram were established based on the selected hub genes. The 45 DEGs were identified and the top 30 hub genes were chosen out for further study. Finally, 11 genes were selected to construct the logistic regression model and nomogram. The receiver operating characteristic (ROC) curve shows that the area under the curve (AUC) value was 0.960 in the training dataset and 0.760 in the validation dataset. A 11-gene diagnostic model was constructed with IL1B, CXCL10, CXCL2, LCN2, MMP12, CXCL9, NOS2, GBP5, FPR1, GBP4 and WARS, which may become potential biomarkers for early diagnosis and targeted therapy of CD.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 4","pages":"339-347"},"PeriodicalIF":1.5,"publicationDate":"2023-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9826363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0