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H9C2 and mToR

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https://read.qxmd.com/read/30798134/tanshinone-iia-protects-against-heart-failure-post-myocardial-infarction-via-ampks-mtor-dependent-autophagy-pathway
#1
Xuefeng Zhang, Qiyan Wang, Xiaoping Wang, Xu Chen, Mingyan Shao, Qian Zhang, Dongqing Guo, Yan Wu, Chun Li, Wei Wang, Yong Wang
Heart failure (HF) leads to an increase in morbidity and mortality globally. Tanshinone IIA is an important traditional Chinese medicine monomer and has been shown to have remarkable protective effect against HF. Autophagy is critically involved in the progression of HF. The effect of Tanshinone IIA on autophagy has not been clarified yet. In this study, left anterior descending (LAD) ligation was used to induce HF model and a hydrogen peroxide-(H2 O2 -)-induced H9C2 cell injury model was established. in vivo, echocardiography results showed that Tanshinone IIA could significantly improve heart function...
February 21, 2019: Biomedicine & Pharmacotherapy
https://read.qxmd.com/read/30734677/histone-deacetylase-inhibition-attenuates-cardiomyocyte-hypoxia-reoxygenation-injury
#2
Aaron M Williams, Wei He, Yongqing Li, Umar F Bhatti, Vahagn C Nikolian, Panpan Chang, Zhigang Chang, Ihab Halaweish, Baoling Liu, Xin Cheng, Hasan B Alam
Cardiac reperfusion injury can have devastating consequences. Histone deacetylase (HDAC) inhibitors are potent cytoprotective agents, but their role in the prevention of cardiac injury remains ill-defined. We sought to determine the therapeutic potential of HDAC inhibitors in an in vitro model of cardiomyocyte hypoxia-reoxygenation (H/R). H9c2 cardiomyocytes were subjected to H/R and treated with various class-specific and pan-HDAC inhibitors in equal concentrations (5μM). Biologic activity of inhibitors was determined, as a proxy for concentration adequacy, by Western blot for acetylated histone H3 and α-tubulin...
February 7, 2019: Current Molecular Medicine
https://read.qxmd.com/read/30551524/long-noncoding-rna-rmrp-upregulation-aggravates-myocardial-ischemia-reperfusion-injury-by-sponging-mir-206-to-target-atg3-expression
#3
Fei Kong, Juan Jin, Xiaolin Lv, Yubo Han, Xue Liang, Yanyu Gao, Xinglin Duan
OBJECTIVE: Coronary heart disease is a common cause of death and disability worldwide and mainly results from myocardial ischemia-reperfusion (I/R) injury. This study aimed to elucidate the roles and possible mechanism of long noncoding RNA Component Of Mitochondrial RNA Processing Endoribonuclease (RMRP) in protecting against ischemic myocardial injury. MATERIAL AND METHODS: The H9c2 cardiomyocytes were cultured under hypoxia condition to induce myocardial injury...
January 2019: Biomedicine & Pharmacotherapy
https://read.qxmd.com/read/30481906/-rosuvastatin-protects-acute-myocardial-infarction-rats-through-autophagy-regulation-via-ampk-signaling
#4
Z C Song, L Chen, D Zhang, S Y Zhang, X Lin
Objective: To investigate the effects of rosuvastatin (RSV)on autophagy and apoptosis of myocardial cells in rats with acute myocardial infarction. Methods: SD rats were divided into control (Sham group), acute myocardial infarction model rats (AMI group), AMI rats treated by RSV with the dose of 5 mg·kg(-1)·d(-1) (RSV group), AMI rats treated by RSV and AMPK inhibitor Compound C at the same time (RSV+ CC group)( n =8) based on simple random sampling methods.Rat myocardial cell line H9c2 was divided into control group, Hypoxia group, Hypoxia+ RSV group, Hypoxia+ RSV+ Compound C group, Hypoxia+ AICAR (AMPK activator)group...
November 20, 2018: Zhonghua Yi Xue za Zhi [Chinese medical journal]
https://read.qxmd.com/read/30431062/mir-181b-5p-suppresses-starvation-induced-cardiomyocyte-autophagy-by-targeting-hspa5
#5
Liuhui Chang, Xiaoming Chai, Peiming Chen, Jianfang Cao, Hong Xie, Jiang Zhu
This study aimed to investigate the role of microRNA‑181b‑5p (miR‑181b‑5p) in starvation‑induced cardiomyocyte autophagy by targeting heat shock protein family A member 5 (Hspa5). For this purpose, H9c2 cardiomyocytes and neonatal rat ventricular myocytes (NRVMs) were glucose‑starved in Earle's Balanced Salt Solution (EBSS) for different periods of time (0, 2, 4, 6 and 8 h). RT‑qPCR analysis was performed to examine the expression of miR‑181b‑5p in the different groups. Immunofluorescence was performed to detect the expression of LC3...
January 2019: International Journal of Molecular Medicine
https://read.qxmd.com/read/30348524/mir-129-5p-inhibits-autophagy-and-apoptosis-of-h9c2-cells-induced-by-hydrogen-peroxide-via-the-pi3k-akt-mtor-signaling-pathway-by-targeting-atg14
#6
Hongbin Zhang, Xiaoqun Zhang, Jun Zhang
Ischemic heart disease (IHD) is a significant cause of cardiovascular diseases. MicroRNAs (miRNAs) have been thought to be critical regulators in the heart diseases. The present study was aimed to investigate the effect of miR-129-5p on the autophagy and apoptosis by targeting ATG14 as well as how miR-129-5p worked through the PI3K/AKT/mTOR signaling pathway in H2 O2 -induced H9c2 cells. H9c2 cells were induced by H2 O2 , after which the expression of miR-129-5p was decreased. Reverse transcription-quantitative polymerase chain reaction (qRT-PCR) was performed to detect the expression level of miR-129-5p in H9c2 cells...
October 19, 2018: Biochemical and Biophysical Research Communications
https://read.qxmd.com/read/30338817/remote-ischemic-postconditioning-alleviates-myocardial-ischemia-reperfusion-injury-by-up-regulating-aldh2
#7
Z-X Zhang, H Li, J-S He, H-J Chu, X-T Zhang, L Yin
OBJECTIVE: The myocardial ischemia/reperfusion (I/R) injury is a significant challenge, and the clinical significance of remote ischemic postconditioning (RIPostC) in cardioprotection has been confirmed. However, the molecular mechanism remains unclear. We aimed to explore the regulatory mechanism of RIPostC in myocardial I/R. MATERIALS AND METHODS: A mouse model of myocardial I/R injury and cell model of oxygen-glucose deprivation (OGD)/re-oxygenation (OGD/R) injury were constructed...
October 2018: European Review for Medical and Pharmacological Sciences
https://read.qxmd.com/read/30283359/lysophosphatidic-acid-is-associated-with-cardiac-dysfunction-and-hypertrophy-by-suppressing-autophagy-via-the-lpa3-akt-mtor-pathway
#8
Jinjing Yang, Jiyao Xu, Xuebin Han, Hao Wang, Yuean Zhang, Jin Dong, Yongzhi Deng, Jingping Wang
Background: Lysophosphatidic acid (LPA), as a phospholipid signal molecule, participates in the regulation of various biological functions. Our previous study demonstrated that LPA induces cardiomyocyte hypertrophy in vitro ; however, the functional role of LPA in the post-infarct heart remains unknown. Growing evidence has demonstrated that autophagy is involved in regulation of cardiac hypertrophy. The aim of the current work was to investigate the effects of LPA on cardiac function and hypertrophy during myocardial infarction (MI) and determine the regulatory role of autophagy in LPA-induced cardiomyocyte hypertrophy...
2018: Frontiers in Physiology
https://read.qxmd.com/read/30223933/cardamonin-protects-against-adverse-cardiac-remodeling-through-mtorc1-inhibition-in-mice-with-myocardial-infarction
#9
Wei You, Zhiming Wu, Fei Ye, Xiangqi Wu
The mTORC1-dependent signaling pathway is mainly involved in the adverse left ventricular remodeling (ALVR) process after myocardial infarction (MI). However, whether mTORC1 inhibition by cardamonin attenuates ALVR after MI is still not reported. Twenty mice were randomly assigned into three groups: sham group (10 ml/kg/day PBS, n=6), model group (MI and 10 ml/kg/day PBS, n=7) and cardamonin-treated group (MI and 20 mg/kg/day cardamonin, n=7). All groups received an intraperitoneal injection accordingly for two weeks...
September 1, 2018: Die Pharmazie
https://read.qxmd.com/read/30031611/recombinant-human-brain-natriuretic-peptide-regulates-pi3k-akt-mtor-pathway-through-lncrna-egot-to-attenuate-hypoxia-induced-injury-in-h9c2-cardiomyocytes
#10
Chengxi Zhang, Sinian Pan, Ayipaxa Aisha, Minawaer Abudoukelimu, Leile Tang, Yesheng Ling
This study aimed to investigate whether recombinant human brain natriuretic peptide (rhBNP) regulated hypoxia-induced injury in H9c2 cardiomyocytes through lncRNA EGOT. H9c2 cardiomyocytes were cultured under normoxia and hypoxia (21% and 3% O2 ) conditions, and whether hypoxia induced injury by assessing cell viability, apoptosis and autophagy. H9c2 cells were then treated with different doses of exogenous rhBNP (200, 600 and 900 nmol/L, respectively) and the effects of rhBNP on hypoxia-induced injury in H9c2 cells as well as the expression of EGOT were studied...
September 10, 2018: Biochemical and Biophysical Research Communications
https://read.qxmd.com/read/29955901/trimetazidine-protects-against-myocardial-ischemia-reperfusion-injury-by-inhibiting-excessive-autophagy
#11
Shiyong Wu, Guanglei Chang, Lei Gao, Dan Jiang, Liyou Wang, Guoxing Li, Xuexiu Luo, Shu Qin, Xueli Guo, Dongying Zhang
Trimetazidine (TMZ) has been demonstrated to have protective effects against myocardial ischemia/reperfusion (MI/R) injury. In the present study, we investigated the effects and the underlying mechanisms of TMZ on autophagy during MI/R in vivo and in vitro. In the in vivo study, an animal model of MI/R was induced by coronary occlusion. TMZ (20 mg/kg/day) protected the rat hearts from MI/R-induced heart failure by increasing ejection fraction and fractional shortening and decreasing end-systolic volume, end-diastolic volume, left ventricular (LV) internal diameter at systole, and LV internal diameter at diastole; it alleviated myocardial injury and oxidative stress by decreasing LDH, creatine kinase MB isoenzyme, ROS, and MDA levels and increasing SOD and glutathione peroxidase levels in plasma...
August 2018: Journal of Molecular Medicine: Official Organ of the "Gesellschaft Deutscher Naturforscher und Ärzte"
https://read.qxmd.com/read/29880088/ginsenoside-rg1-protects-cardiomyocytes-from-hypoxia-induced-injury-through-the-pi3k-akt-mtor-pathway
#12
Liang Qin, Shuxia Fan, Rongbo Jia, Yongxuan Liu
AIM: Myocardial ischemia (MI) is a leading cause of morbidity and mortality which makes the prevention and control of MI tremendously important. We aimed to explore the functional roles of ginsenoside (Gin) Rg1 in cardiomyocytes under hypoxia and to clarify underlying mechanisms. MAIN METHODS: Hypoxia-induced H9c2 cell injury was evaluated by alterations of cell viability, apoptosis and autophagy. Then, effects of Gin Rg1 on hypoxia-induced cell injury were measured...
June 1, 2018: Die Pharmazie
https://read.qxmd.com/read/29849901/exendin-4-and-liraglutide-attenuate-glucose-toxicity-induced-cardiac-injury-through-mtor-ulk1-dependent-autophagy
#13
Wei Yu, Wenliang Zha, Jun Ren
Mitochondrial injury and defective autophagy are common in diabetic cardiomyopathy. Recent evidence supports benefits of glucagon-like peptide-1 (GLP-1) agonists exendin-4 (Exe) and liraglutide (LIRA) against diabetic cardiomyopathy. This study was designed to examine the effect of Exe and LIRA on glucose-induced cardiomyocyte and mitochondrial injury, oxidative stress, apoptosis, and autophagy change. Cardiomyocytes isolated from adult mice and H9c2 myoblast cells were exposed to high glucose (HG, 33 mM) with or without Exe or LIRA...
2018: Oxidative Medicine and Cellular Longevity
https://read.qxmd.com/read/29786755/cardiac-progenitor-cell%C3%A2-derived-exosomes-promote-h9c2-cell-growth-via-akt-mtor-activation
#14
Shentang Li, Jie Jiang, Zuocheng Yang, Zhuoying Li, Xing Ma, Xin Li
Exosomes are cell‑derived vesicles released from a variety of mammalian cells that are involved in cell‑to‑cell signalling. It has been reported that cardiac progenitor cells (CPCs) derived from an adult heart are one of the most promising stem cell types for cardioprotection and repair. The mammalian target of rapamycin (mTOR) signalling pathway is a pivotal regulator in CPCs, therefore, CPC‑derived exosomes were used in the present study to investigate whether it can promote H9C2 cell growth through the protein kinase B (PKB, or Akt)/mTOR signalling pathway...
September 2018: International Journal of Molecular Medicine
https://read.qxmd.com/read/29763685/autophagy-plays-a-pro-survival-role-against-methamphetamine-induced-apoptosis-in-h9c2-cells
#15
Chao Zhao, Yong Mei, Xufeng Chen, Lei Jiang, Yunfei Jiang, Xu Song, Hang Xiao, Jingsong Zhang, Jun Wang
Methamphetamine (METH) is a commonly abused psychostimulant that can induce severe neurotoxicity. Cardiovascular injury caused by METH has recently gained increasing attention; however, the underlying mechanisms remain unclear. As autophagy has been shown to be associated with cell injury, the association between autophagy and METH-mediated cell apoptosis was investigated in the present study. METH treatment significantly increased the expression of two key autophagy proteins, i.e., Beclin-1 and LC3-II, in the cardiomyocyte cell line H9C2...
September 15, 2018: Toxicology Letters
https://read.qxmd.com/read/29745968/the-long-noncoding-rna-thril-knockdown-protects-hypoxia-induced-injuries-of-h9c2-cells-through-regulating-mir-99a
#16
Jingwen Xia, Nianxin Jiang, Yansong Li, Yong Wei, Xuan Zhang
BACKGROUND: Myocardial infarction (MI) is a leading cause of disease with high morbidity and mortality worldwide. Recent studies have revealed that long non-coding RNAs (lncRNAs) are involved in heart disease pathogenesis. This study aimed to investigate the effect and the molecular basis of THRIL on hypoxia-injured H9C2 cells. METHODS: THRIL, miR-99a and Brahma-related gene 1 (Brg1) expression in H9C2 cells were altered by transient transfections. The cells were subjected to hypoxia for 4 h, and then the levels of THRIL, miR-99a and Brg1 were investigated...
May 10, 2018: Cardiology Journal
https://read.qxmd.com/read/29734265/vaspin-prevents-tumor-necrosis-factor-%C3%AE-induced-apoptosis-in-cardiomyocytes-by-promoting-autophagy
#17
Xuan Ke, Yanqin Hao, Bingong Li, Jin Zou, Xuelian Li, Chunying Wei, Fuyou Liu, Zhiyong Zhang
Visceral adipose tissue-derived serine protease inhibitor (Vaspin) is an adipocytokine that has been shown to exert anti-inflammatory effects and inhibits apoptosis under diabetic conditions. This study was designed to investigate the impact of vaspin on autophagy in tumor necrosis factor (TNF)-α-induced injury in cardiomyocytes and its cardioprotective effects in the pathogenesis of diabetic cardiomyopathy (DCM). H9C2 cells were treated with TNF-α with or without vaspin in vitro. Tumor necrosis factor-α treatment inhibited autophagy and promoted apoptosis in H9C2 cells after stimulating for 24 hours...
May 2018: Journal of Cardiovascular Pharmacology
https://read.qxmd.com/read/29723857/resveratrol-modulates-apoptosis-and-autophagy-induced-by-high-glucose-and-palmitate-in-cardiac-cells
#18
Kui Xu, Xiu-Fen Liu, Zhi-Qiang Ke, Qing Yao, Shuang Guo, Chao Liu
BACKGROUND/AIMS: Diabetic cardiomyopathy is associated with increased apoptosis and suppressed autophagy in cardiac cells. The polyphenol resveratrol has shown beneficial effects in various cardiovascular diseases. This study investigated if resveratrol protected cardiac cells by modulating apoptosis and autophagy in the context of diabetes. METHODS: H9c2 cardiac myoblast cells were exposed to high glucose combined with palmitate. Autophagy was evaluated by estimating LC3-II/I ratio, P62 protein levels, and LC3 fluorescent puncta...
2018: Cellular Physiology and Biochemistry
https://read.qxmd.com/read/29710553/microrna-210-aggravates-hypoxia-induced-injury-in-cardiomyocyte-h9c2-cells-by-targeting-cxcr4
#19
Min Feng, Zongqing Li, Dong Wang, Fang Wang, Chenyan Wang, Chunfang Wang, Faming Ding
BACKGROUND: Myocardial infarction (MI), a leading cause of mortality, is identified as the myocardial necrosis due to prolonged ischemia. Hypoxia, resulting from ischemia, induces cell apoptosis during MI. Since miR-210 is a hypoxia inducible factor, we aimed to explore the functional role of miR-210 in hypoxic H9c2 cells. METHODS: Hypoxia-induced cell injury was evaluated according to cell viability, apoptosis and expression of apoptosis-associated proteins. miR-210 expression after hypoxia was tested...
June 2018: Biomedicine & Pharmacotherapy
https://read.qxmd.com/read/29682889/fkbp12-6-protects-heart-from-angii-induced-hypertrophy-through-inhibiting-ca-2-calmodulin-mediated-signalling-pathways-in-vivo-and-in-vitro
#20
Yun-Fei Xiao, Zhi-Xiong Zeng, Xiao-Hui Guan, Ling-Fang Wang, Chan-Juan Wang, Huidong Shi, Weinian Shou, Ke-Yu Deng, Hong-Bo Xin
We previously observed that disruption of FK506-binding protein 12.6 (FKBP12.6) gene resulted in cardiac hypertrophy in male mice. Studies showed that overexpression of FKBP12.6 attenuated thoracic aortic constriction (TAC)-induced cardiac hypertrophy in mice, whereas the adenovirus-mediated overexpression of FKBP12.6 induced hypertrophy and apoptosis in cultured neonatal cardiomyocytes, indicating that the role of FKBP12.6 in cardiac hypertrophy is still controversial. In this study, we aimed to investigate the roles and mechanisms of FKBP12...
July 2018: Journal of Cellular and Molecular Medicine
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