General physiology and biophysics最新文献_第7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

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

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":"42 3","pages":"285-295"},"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

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":"42 3","pages":"241-250"},"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

Effects of the acute administration of delta-opioid receptor ligands on the excitability of rat hippocampal glutamate and brainstem monoamine neurons in vivo. 阿片受体配体急性给药对大鼠海马谷氨酸和脑干单胺神经元兴奋性的影响。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023010

Daniil Grinchii, Lubica Lacinova, Eliyahu Dremencov

{"title":"Effects of the acute administration of delta-opioid receptor ligands on the excitability of rat hippocampal glutamate and brainstem monoamine neurons in vivo.","authors":"Daniil Grinchii, Lubica Lacinova, Eliyahu Dremencov","doi":"10.4149/gpb_2023010","DOIUrl":"https://doi.org/10.4149/gpb_2023010","url":null,"abstract":"It was previously reported that the delta opioid receptor (DOR) agonist SNC80 and antagonist naltrindole modulate the excitability of hippocampal glutamate neurons in primary cultures. The present study aimed to investigate the acute effects of these ligands on the firing activity of hippocampal cornu ammonis 1/3 (CA1/3) glutamate, dorsal raphe nucleus (DRN) serotonin (5-HT), locus coeruleus (LC) noradrenaline, and ventral tegmental area (VTA) dopamine neurons in in vivo conditions. Adult Wistar male rats were used. SNC80 and naltrindole were administered intravenously. Neuronal firing activity was assessed using extracellular single-unit electrophysiology. SNC80, administered first at 1-3 mg/kg, dose-dependently inhibited CA1/3 glutamate, DRN 5-HT, and VTA dopamine neurons. Naltrindole, administered at 1-3 mg/kg after SNC80, did not have any additional effect. Naltrindole, administered first at 1-3 mg/kg, stimulated DRN 5-HT neurons in a dose-dependent manner; this stimulation was dose-dependently reversed by 1-3 mg/kg of SNC80. SNC80 and naltrindole inhibited LC noradrenaline neurons when only they were co-administered at 3 mg/kg, and only when SNC80 was administered first. In conclusion, DOR ligands alter the firing activity of hippocampal glutamate and brainstem monoamine neurons in in vivo conditions. The psychoactive effects of DOR ligands, reported in previous studies, might be explained, at least in part, by their ability to modulate the firing activity of hippocampal glutamate and brainstem monoamine neurons.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 3","pages":"273-283"},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9409038","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

Chloroquine inhibits vasodilation induced by ATP-sensitive potassium channels in isolated rat aorta. 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 : 2023-05-01 DOI: 10.4149/gpb_2023008

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

{"title":"Chloroquine inhibits vasodilation induced by ATP-sensitive potassium channels in isolated rat aorta.","authors":"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","doi":"10.4149/gpb_2023008","DOIUrl":"https://doi.org/10.4149/gpb_2023008","url":null,"abstract":"This study examined the effect of chloroquine on vasodilation induced by levcromakalim in isolated endothelium-denuded rat aortas and clarified the underlying mechanisms. We examined the effects of chloroquine, hydroxychloroquine, lipid emulsion, reactive oxygen species (ROS) scavenger N-acetyl-ʟ-cysteine (NAC), and KATP channel inhibitor glibenclamide on levcromakaliminduced vasodilation. The effects of chloroquine, hydroxychloroquine, NAC, and levcromakalim on membrane hyperpolarization and ROS production were examined in aortic vascular smooth muscle cells (VSMCs). Chloroquine inhibited levcromakalim-induced vasodilation more than hydroxychloroquine. NAC attenuated chloroquine-mediated inhibition of levcromakalim-induced vasodilation, while lipid emulsion had no effect. Glibenclamide eliminated levcromakalim-induced vasodilation in aortas pretreated with chloroquine. Chloroquine and hydroxychloroquine inhibited levcromakalim-induced membrane hyperpolarization in VSMCs. Chloroquine and hydroxychloroquine both produced ROS, but chloroquine produced more. NAC inhibited chloroquine-induced ROS production in VSMCs. Collectively, these results suggest that, partially through ROS production, chloroquine inhibits levcromakalim-induced vasodilation. In addition, chloroquine-induced KATP channel-induced vasodilation impairment was not restored by lipid emulsion.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 3","pages":"297-306"},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9831230","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

The effect of 12 week-maximum fat oxidation intensity (FATmax) exercise on microvascular function in obese patients with nonalcoholic fatty liver disease and its mechanism. 12周最大脂肪氧化强度(FATmax)运动对肥胖非酒精性脂肪肝患者微血管功能的影响及其机制

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023004

Ruiqi Yang, Li Wan, Huan Zhu, Yong Peng

{"title":"The effect of 12 week-maximum fat oxidation intensity (FATmax) exercise on microvascular function in obese patients with nonalcoholic fatty liver disease and its mechanism.","authors":"Ruiqi Yang, Li Wan, Huan Zhu, Yong Peng","doi":"10.4149/gpb_2023004","DOIUrl":"https://doi.org/10.4149/gpb_2023004","url":null,"abstract":"Fifty-four obese patients with non-alcoholic fatty liver disease (NAFLD) were selected for this study were randomly divided into an exercise group (16 men and 11 women, mean age 21.3 ± 1.0) and control group (16 men and 11 women, mean age 21.8 ± 0.8). The exercise group underwent a 12-week FATmax exercise intervention, while the control group did not engage in any type of systematic physical activity. The controlled diet was given to both groups. After the test, the microvascular reactivity of the exercise group was significantly higher than that of the control group (p < 0.05). After the experiment, the concentration of malondialdehyde (MDA), the activity of catalase (CAT) and the activity of exercise group were significantly lower than those of the control group (p < 0.05); and in contrast the activities of total superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) were significantly higher than those of the control group (p< 0.05). The change in microcirculation function caused by 12-week FATmax intensity exercise may have an interaction mechanism with oxidative stress and antioxidant system function, and may improve the microvascular reactivity of obese NAFLD patients. In addition, also may improve of oxidative stress and antioxidant system functions.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 3","pages":"251-262"},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9352004","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 protective effects of glutamine against bronchopulmonary dysplasia are associated with MKP-1/MAPK/cPLA2 signalingmediated NF-kappaB pathway. 谷氨酰胺对支气管肺发育不良的保护作用与MKP-1/MAPK/cPLA2信号介导的NF-kappaB通路有关。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-05-01 DOI: 10.4149/gpb_2023006

Chouhui Xuan, Can Jin, Zhengyong Jin, Yongxue Chi

{"title":"The protective effects of glutamine against bronchopulmonary dysplasia are associated with MKP-1/MAPK/cPLA2 signalingmediated NF-kappaB pathway.","authors":"Chouhui Xuan, Can Jin, Zhengyong Jin, Yongxue Chi","doi":"10.4149/gpb_2023006","DOIUrl":"https://doi.org/10.4149/gpb_2023006","url":null,"abstract":"Glutamine is proven to have potential therapeutic effects on decreasing hyperoxia-induced acute pulmonary injury. The aim of this study is to investigate the effects and mechanism of glutamine on bronchopulmonary dysplasia (BPD) induced by hyperoxia in rat alveolar type II epithelial cells (AECIIs) RLE-6TN. Following hyperoxia induction and glutamine treatment, ROS levels were detected by DCFH-DA assay and TUNEL staining was performed to detect cell apoptosis. The levels of inflammatory indicators and expression of apoptosis-related proteins were detected through ELISA and Western blot, respectively. Besides, the expression of related proteins in mitogen-activated protein kinase phosphatase-1 (MKP-1)/mitogen-activated protein kinases (MAPK)/cytoplasmic phospholipase A2 (cPLA2) signaling was also detected by Western blot. To further analyze the role of MKP-1/MAPK/cPLA2 signaling, MKP-1 was silenced and anisomycin was used to treat cells, respectively. It was shown that glutamine significantly decreased inflammation, oxidative stress and apoptosis in hyperoxia-induced cells while MKP-1 interference and anisomycin were able to reverse these effects, suggesting that the protective effects of glutamine on BPD induced by hypoxia were related to MKP-1/MAPK/cPLA2 signaling. To sum up, glutamine protected against BPD by decreasing inflammation, oxidative stress and apoptosis via MKP-1/MAPK/cPLA2 signaling.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 3","pages":"229-239"},"PeriodicalIF":1.5,"publicationDate":"2023-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9356781","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

Hypoxic cardiomyocyte-derived exosomes regulate cardiac fibroblast activation, apoptosis, migration and ferroptosis through miR-208a/b. 缺氧心肌细胞来源的外泌体通过miR-208a/b调控心肌成纤维细胞活化、凋亡、迁移和铁下垂。

IF 1.5 4区生物学

General physiology and biophysics Pub Date : 2023-03-01 DOI: 10.4149/gpb_2022061

Ying Guo, Zi-Dong Bie, Xi Li

{"title":"Hypoxic cardiomyocyte-derived exosomes regulate cardiac fibroblast activation, apoptosis, migration and ferroptosis through miR-208a/b.","authors":"Ying Guo, Zi-Dong Bie, Xi Li","doi":"10.4149/gpb_2022061","DOIUrl":"https://doi.org/10.4149/gpb_2022061","url":null,"abstract":"Studies have found that cardiomyocytes and cardiac fibroblasts (CFs) can communicate through exosomes, thereby affecting each other's biological functions, but there are few studies on the mechanism. miR-208a/b are specifically expressed in the heart and highly expressed in exosomes derived from various myocardial diseases. Hypoxia induced cardiomyocytes to secrete exosomes (H-Exo) with high expression of miR-208a/b. When H-Exo were added to CFs for co-culture, it was found that CFs took up exosomes, thereby upregulating the expression of miR-208a/b. H-Exo significantly promoted the viability and migration of CFs, enhanced the expression of α-SMA, collagen I and III, and promoted the secretion of collagen I and III. miR-208a or/and miR-208b inhibitors significantly attenuated the effects of H-Exo on CF biological functions. miR-208a/b inhibitors significantly enhanced the levels of apoptosis and caspase-3 activity in CFs, while H-Exo significantly attenuated the pro-apoptotic effects of miR-208a/b inhibitors. Further treatment of CFs with ferroptosis inducer Erastin found that H-Exo further enhanced the accumulation of ROS, MDA and Fe2+, the main indicators of ferroptosis, and inhibited the expression of GPX4, a key regulator of ferroptosis. miR-208a or/and miR-208b inhibitors significantly attenuated the effects of Erastin and H-Exo on ferroptosis. In conclusion, hypoxic cardiomyocyte-derived exosomes can regulate the biological functions of CFs through highly expressed miR-208a/b.","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 2","pages":"149-158"},"PeriodicalIF":1.5,"publicationDate":"2023-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9256564","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