scholarly journals Retracted: Knockdown of MicroRNA-122 Protects H9c2 Cardiomyocytes from Hypoxia-Induced Apoptosis and Promotes Autophagy

2021 ◽  
Vol 27 ◽  
Author(s):  
Zaiwei Zhang ◽  
Hu Li ◽  
Shasha Chen ◽  
Ying Li ◽  
Zhiyuan Cui ◽  
...  
Keyword(s):  
H9c2 Cardiomyocytes ◽  
Induced Apoptosis

MicroRNA-34a regulates high glucose-induced apoptosis in H9c2 cardiomyocytes

2013 ◽  
Vol 33 (6) ◽  
pp. 834-839 ◽  
Author(s):  
Fang Zhao ◽  
Bo Li ◽  
Yin-zhi Wei ◽  
Bin Zhou ◽  
Han Wang ◽  
...  
Keyword(s):  
High Glucose ◽  
H9c2 Cardiomyocytes ◽  
Induced Apoptosis

(−)-Epicatechin-3-gallate (a polyphenol from green tea) potentiates doxorubicin-induced apoptosis in H9C2 cardiomyocytes

2015 ◽  
Vol 37 (10) ◽  
pp. 1937-1943 ◽  
Author(s):  
Yi Cai ◽  
Hui-Qi Hong ◽  
Li Zhao ◽  
Yue-Peng Cai ◽  
Yuan Qin
Keyword(s):  
Green Tea ◽  
H9c2 Cardiomyocytes ◽  
Induced Apoptosis

Ser9 phosphorylation of mitochondrial GSK-3β is a primary mechanism of cardiomyocyte protection by erythropoietin against oxidant-induced apoptosis

2008 ◽  
Vol 295 (5) ◽  
pp. H2079-H2086 ◽  
Author(s):  
Katsuhiko Ohori ◽  
Tetsuji Miura ◽  
Masaya Tanno ◽  
Takayuki Miki ◽  
Takahiro Sato ◽  
...  
Keyword(s):  
Fluorescent Protein ◽  
Oxidant Stress ◽  
Dependent Manner ◽  
Phosphatidylinositol 3 Kinase ◽  
H9c2 Cardiomyocytes ◽  
Gsk 3Β ◽  
Induced Apoptosis ◽  
Green Fluorescent ◽  
Interfering Rna

The aim of this study was to determine the role of GSK-3β in cardiomyocyte protection afforded by erythropoietin (EPO) against oxidant stress-induced apoptosis. Treatment with EPO (10 units/ml) induced Ser473 phosphorylation of Akt and Ser9 phosphorylation of GSK-3β and significantly reduced the proportion of apoptotic H9c2 cardiomyocytes after exposure to H2O2 from 38.3 ± 2.7% to 26.0 ± 2.9%. This protection was not detected in cells transfected with constitutively active GSK-3β (S9A), which lacks Ser9 for inhibitory phosphorylation. The antiapoptotic effect of EPO was mimicked completely by GSK-3β knockdown using small interfering RNA and partly by the transfection with kinase-deficient GSK-3β (K85R). The level of colocalization of intracellular GSK-3β with mitochondria assessed by enhanced green fluorescent protein-tagged GSK-3β or immunocytochemistry was not altered by EPO treatment. However, EPO increased the level of Ser9-phospho-GSK-3β colocalized with mitochondria by 50% in a phosphatidylinositol 3-kinase-dependent manner. Mitochondrial translocation of Bcl-2-associated X protein (BAX) after exposure to H2O2 was inhibited by EPO pretreatment and by GSK-3β knockdown. These results suggest that the suppression of GSK-3β activity by Akt-mediated Ser9 phosphorylation in the mitochondria affords cardiomyocytes tolerance against oxidant-induced apoptosis, possibly by inhibiting the access of BAX to the mitochondria.

scholarly journals GRK5 is an Essential Co-repressor for Cardiac Mineralocorticoid Receptor Antagonism induced by Finerenone but not Eplerenone

2020 ◽  
Author(s):  
Victoria L. Desimine ◽  
Jennifer Ghandour ◽  
Natalie Cora ◽  
Celina M. Pollard ◽  
Rachel Valiente ◽  
...  
Keyword(s):  
Mineralocorticoid Receptor ◽  
Transcriptional Activity ◽  
Ventricular Myocytes ◽  
Neonatal Rat ◽  
Human Heart Failure ◽  
Cardiac Mr ◽  
Inverse Agonism ◽  
Mineralocorticoid Receptor Antagonism ◽  
H9c2 Cardiomyocytes ◽  
Induced Apoptosis

Background: In the heart, aldosterone (Aldo) binds the mineralocorticoid receptor (MR) to exert damaging, adverse remodeling-promoting effects. We recently showed that G protein-coupled receptor (GPCR)-kinase (GRK)-5 blocks the cardiac MR by directly phosphorylating it, thereby repressing its transcriptional activity. MR antagonist (MRA) drugs block the cardiac MR reducing morbidity and mortality of advanced human heart failure. Non-steroidal MRAs, such as finerenone, may provide better cardio-protection against Aldo than classic, steroidal MRAs, like spironolactone and eplerenone. Herein, we sought to investigate potential differences between finerenone and eplerenone at engaging GRK5-dependent cardiac MR phosphorylation and subsequent blockade. Methods: We used the cardiomyocyte cell line H9c2 and neonatal rat ventricular myocytes (NRVMs). Results: GRK5 phosphorylates the MR in H9c2 cardiomyocytes in response to finerenone but not to eplerenone. Unlike eplerenone, finerenone alone potently and efficiently suppresses cardiac MR transcriptional activity, thus displaying inverse agonism. GRK5 is necessary for finerenone`s inverse agonism, since GRK5 genetic deletion renders finerenone incapable of blocking cardiac MR transcriptional activity. Eplerenone alone does not fully suppress cardiac MR basal activity regardless of GRK5 expression levels. Finally in NRVMs, GRK5 is necessary for the anti-apoptotic and anti-fibrotic effects of both finerenone and eplerenone against Aldo, as well as for the higher efficacy and potency of finerenone at blocking Aldo-induced apoptosis and fibrosis. Conclusions: Finerenone, but not eplerenone, induces GRK5-dependent cardiac MR inhibition, which underlies, at least in part, its higher potency and efficacy, compared to eplerenone, as an MRA in the heart. GRK5 acts as a co-repressor of the cardiac MR and is essential for efficient MR antagonism in the myocardium.

scholarly journals Triterpenoid saponins from Ilex cornuta protect H9c2 cardiomyocytes against H2O2-induced apoptosis by modulating Ezh2 phosphorylation

2021 ◽  
Vol 269 ◽  
pp. 113691
Author(s):  
Danhong Yu ◽  
Zengyan Zhu ◽  
Mei Wang ◽  
Xinyuan Ding ◽  
Huan Gui ◽  
...  
Keyword(s):  
Triterpenoid Saponins ◽  
H9c2 Cardiomyocytes ◽  
Ilex Cornuta ◽  
Induced Apoptosis

scholarly journals Ginsenoside RK3 Prevents Hypoxia-Reoxygenation Induced Apoptosis in H9c2 Cardiomyocytes via AKT and MAPK Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Jing Sun ◽  
Guibo Sun ◽  
Xiangbao Meng ◽  
Hongwei Wang ◽  
Min Wang ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Mapk Pathway ◽  
Heart Diseases ◽  
Reperfusion Therapy ◽  
Ischemic Heart Diseases ◽  
H9c2 Cardiomyocytes ◽  
Cardioprotective Effects ◽  
Underlying Mechanisms ◽  
Induced Apoptosis ◽  
Hypoxia Reoxygenation

Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), but further injury induced by rapidly initiating reperfusion of the heart is often encountered in clinical practice. Ginsenoside RK3 (RK3) is reportedly present in the processed Radix notoginseng that is often used as a major ingredient of the compound preparation for ischemic heart diseases. This study aimed to investigate the possible protective effect of RK3 against hypoxia-reoxygenation (H/R) induced H9c2 cardiomyocytes damage and its underlying mechanisms. Our results showed that RK3 pretreatment caused increased cell viability and decreased levels of LDH leakage compared with the H/R group. Moreover, RK3 pretreatment inhibited cell apoptosis, as evidenced by decreased caspase-3 activity, TUNEL-positive cells, and Bax expression, as well as increased Bcl-2 level. Further mechanism investigation revealed that RK3 prevented H9c2 cardiomyocytes injury and apoptosis induced by H/R via AKT/Nrf-2/HO-1 and MAPK pathways. These observations indicate that RK3 has the potential to exert cardioprotective effects against H/R injury, which might be of great importance to clinical efficacy for AMI treatment.

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