General physiology and biophysics最新文献_第5页

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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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":null,"pages":null},"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

Knockdown of lncRNA NKILA suppresses sevoflurane-induced neuronal cell injury partially by targeting miR-205-5p/ELAVL1 axis. lncRNA的敲低NKILA通过靶向miR-205-5p/ELAVL1轴部分抑制七氟烷诱导的神经元细胞损伤。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023007

Yilong Zhang, Changbai Chen

{"title":"Knockdown of lncRNA NKILA suppresses sevoflurane-induced neuronal cell injury partially by targeting miR-205-5p/ELAVL1 axis.","authors":"Yilong Zhang, Changbai Chen","doi":"10.4149/gpb_2023007","DOIUrl":"https://doi.org/10.4149/gpb_2023007","url":null,"abstract":"Sevoflurane (Sev) is a wildly used volatile anesthetic agent that induces neurotoxicity. Long non-coding RNAs (lncRNAs) have been demonstrated to be involved in Sev-induced neuronal injury. Here, we investigated the role of NF-kappaB-interacting lncRNA (NKILA) in Sev-treated human cortical neurons (HCN). From RT-qPCR, Sev dose-dependently increased HCN NKILA transcript expression. Neurotoxicity of Sev was detected using MTT, flow cytometry, Western blotting, and inflammatory mediator assays. Consequently, Sev reduced HCN viability and levels of Bcl-2, SOD, and GSH in HCN, and promoted HCN apoptosis rate and levels of cleaved-caspase-3, Bax, MDA, TNF-α, IL-6, and IL-1β. Silencing NKILA suppressed Sev-induced above effects. DIANA and starbase databases predicted the potential target relationship between miR-205-5p and NKILA or embryonic lethal abnormal vision-like 1 (ELAVL1); dual-luciferase and RIP confirmed these interactions. NKILA could increase ELAVL1 expression by regulating miR-205-5p. miR-205-5p overexpression and ELAVL1 knockdown could mimic effects of NKILA silencing in Sev-induced HCN. Deleting miR-205-5p and restoring ELAVL1 respectively abolished the neuroprotective effect of NKILA knockdown and miR-205-5p upregulation under Sev anesthesia. In conclusion, Sev induced neuronal cell apoptosis, inflammatory response and oxidative stress through NKILA/miR- 205-5p/ELAVL1 axis and caspase-3 and Bax/Bcl-2 pathway. Inhibiting NKILA might be a potential therapeutic strategy for Sev neurotoxicity.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9409033","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

MicroRNA-21-3p/Rcan1 signaling axis affects apoptosis of cardiomyocytes of sepsis rats. MicroRNA-21-3p/Rcan1信号轴影响脓毒症大鼠心肌细胞凋亡。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2022066

Mingwei Gong, Li Tao, Xia Li

{"title":"MicroRNA-21-3p/Rcan1 signaling axis affects apoptosis of cardiomyocytes of sepsis rats.","authors":"Mingwei Gong, Li Tao, Xia Li","doi":"10.4149/gpb_2022066","DOIUrl":"https://doi.org/10.4149/gpb_2022066","url":null,"abstract":"Accumulating evidence has reported the role of microRNA-21-3p (miR-21-3p) in sepsis, and our objective was to discuss the effect of the miR-21-3p/regulator of calcineurin 1 (Rcan1) axis on cardiomyocyte apoptosis of septic rats. miR-21-3p and Rcan1 expression in myocardial tissues of lipopolysaccharide (LPS)-treated rats and LPS-treated H9c2 cardiomyocytes was determined. The influences of downregulating miR-21-3p or upregulating Rcan1 in cardiomyocyte apoptosis of LPS-treated rats and LPS-treated H9c2 cardiomyocytes were then evaluated. The target relation between Rcan1 and miR-21-3p was verified. It was observed that miR-21-3p was elevated and Rcan1 was reduced in LPS-treated rats and LPS-treated H9c2 cardiomyocytes. Downregulating miR-21-3p or upregulating Rcan1 could suppress cardiomyocyte apoptosis of LPS-treated rats and LPS-treated H9c2 cardiomyocytes. Based on the dual-luciferase activity assay, miR-21-3p was directly targeted Rcan1 in H9c2 cardiomyocytes. In the rescue experiment, the LPS+miR-21-3p inhibitor+si-Rcan1 group enhanced the apoptosis of H9c2 cardiomyocytes in comparison to the LPS+miR-21-3p inhibitor+si-NC group. Together, our findings identify that the miR-21-3p/Rcan1 axis may affect apoptosis of cardiomyocytes in sepsis, which provides a new idea for understanding the potential mechanism of sepsis.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9356777","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

Granulocyte-colony stimulating factor mediates neovascularization in acellular dermal matrix-transplanted areas by promoting endothelial progenitor cell homing. 粒细胞集落刺激因子通过促进内皮祖细胞归巢介导脱细胞真皮基质移植区新生血管的形成。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023002

Jun Wang, Xuan Liao, Xiao Jiang, Hongwei Liu

{"title":"Granulocyte-colony stimulating factor mediates neovascularization in acellular dermal matrix-transplanted areas by promoting endothelial progenitor cell homing.","authors":"Jun Wang, Xuan Liao, Xiao Jiang, Hongwei Liu","doi":"10.4149/gpb_2023002","DOIUrl":"https://doi.org/10.4149/gpb_2023002","url":null,"abstract":"Acellular dermal matrix (ADM) is an ideal material for tissue engineering skin construction. Accelerating the vascularization of ADM is of great significance for improving the survival of skin transplantation. The purpose of this study is to investigate the function of granulocyte-colony stimulating factor (G-CSF) in endothelial progenitor cells (EPCs)-mediated neovascularization in ADM-transplanted skin area. Male Kunming mice were subcutaneous injected with 10 μg/kg GCSF at 5 days before skin in situ replantation or porcine ADM transplantation. The surrounding tissues of implanted skin or venous blood was collected from the mice before the operation, and after the operation for 48 h, 72 h, 1 week, and 2 weeks, respectively. Cells co-expressing EPC markers, CD133, CD34, and Flk-1 were detected by flow cytometry. Immunohistochemistry of BrdU was performed to evaluate neovascularization in ADM-transplanted skin area. The results showed that G-CSF treatment increased the number of CD133+-CD34+ cells and CD133+-Flk-1+ cells in ADMimplanted area as well as the number of CD34+-Flk-1+ cells in peripheral blood. Likewise, G-CSF also increased the number of capillaries in ADM-transplanted areas. To sum up, G-CSF mobilizes EPC migration from bone marrow to peripheral blood and homing to wound sites, thus inducing neovascularization in ADM-transplanted areas.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9409036","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

Cholecalciferol affects cardiac proteins regulating malonyl-CoA availability and intracellular calcium level. 胆钙化醇影响调节丙二酰辅酶a可用性和细胞内钙水平的心脏蛋白。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023005

Tamara Ivkovic, Snezana Tepavcevic, Snjezana Romic, Mojca Stojiljkovic, Milan Kostic, Jelena Stanisic, Goran Koricanac, Tijana Culafic

{"title":"Cholecalciferol affects cardiac proteins regulating malonyl-CoA availability and intracellular calcium level.","authors":"Tamara Ivkovic, Snezana Tepavcevic, Snjezana Romic, Mojca Stojiljkovic, Milan Kostic, Jelena Stanisic, Goran Koricanac, Tijana Culafic","doi":"10.4149/gpb_2023005","DOIUrl":"https://doi.org/10.4149/gpb_2023005","url":null,"abstract":"Cholecalciferol improves insulin signaling and glucose metabolism in the heart and reduces circulating non-esterified fatty acids. Cholecalciferol effects on the cardiac fatty acid (FA) metabolism and the consequences on calcium handling were examined. Blood lipid profile was determined. Western blot and qRT-PCR were used to examine protein and mRNA expression. Cholecalciferoltreated rats had increased acetyl CoA carboxylase 2 protein expression and decreased expression of malonyl CoA decarboxylase. In addition, the expression of uncoupling protein 3 was elevated. Also, the level of peroxisome proliferator-activated receptor-gamma coactivator in the nucleus of heart cells was increased along with the level of sarcoplasmic/endoplasmic reticulum Ca2+ATPase in the microsomal fraction. In parallel, the L-type calcium channel and ryanodine receptor expression was reduced. In the heart of healthy rats, cholecalciferol affects proteins regulating malonyl CoA availability and intracellular Ca2+ handling proteins.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":null,"pages":null},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9409037","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