The role of ?1 integrin in spreading and myofibrillogenesis in neonatal rat cardiomyocytes in vitro

1992 ◽  
Vol 21 (2) ◽  
pp. 87-100 ◽  
Author(s):  
Lula L. Hilenski ◽  
Ma Xuehui ◽  
Nancy Vinson ◽  
Louis Terracio ◽  
Thomas K. Borg
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Role of Calcium-Activated Neutral Protease (Calpain) in Cell Death in Cultured Neonatal Rat Cardiomyocytes During Metabolic Inhibition

1995 ◽  
Vol 76 (6) ◽  
pp. 1071-1078 ◽  
Author(s):  
Douwe E. Atsma ◽  
E.M. Lars Bastiaanse ◽  
Anastazia Jerzewski ◽  
Lizet J.M. Van der Valk ◽  
Arnoud Van der Laarse
Keyword(s):  
Cell Death ◽  
Metabolic Inhibition ◽  
Neonatal Rat ◽  
Neutral Protease ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

scholarly journals Aldosterone increases T-type calcium channel expression and in vitro beating frequency in neonatal rat cardiomyocytes

2005 ◽  
Vol 67 (2) ◽  
pp. 216-224 ◽  
Author(s):  
N LALEVEE ◽  
M REBSAMEN ◽  
S BARRERELEMAIRE ◽  
E PERRIER ◽  
J NARGEOT ◽  
...  
Keyword(s):  
Calcium Channel ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Channel Expression ◽  
Beating Frequency

scholarly journals Ginsenoside Rb1 Protects Neonatal Rat Cardiomyocytes from Hypoxia/Ischemia Induced Apoptosis and Inhibits Activation of the Mitochondrial Apoptotic Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Xu Yan ◽  
Jinwen Tian ◽  
Hongjin Wu ◽  
Yuna Liu ◽  
Jianxun Ren ◽  
...  
Keyword(s):  
Caspase 3 ◽  
Neonatal Rat ◽  
Ginsenoside Rb1 ◽  
Caspase 9 ◽  
Apoptotic Pathway ◽  
Rat Cardiomyocytes ◽  
Mitochondrial Apoptotic Pathway ◽  
Neonatal Rat Cardiomyocytes ◽  
Hypoxia Ischemia

Aim. To investigate the effect of Ginsenoside Rb1 (GS-Rb1) on hypoxia/ischemia (H/I) injury in cardiomyocytesin vitroand the mitochondrial apoptotic pathway mediated mechanism.Methods. Neonatal rat cardiomyocytes (NRCMs) for the H/I groups were kept in DMEM without glucose and serum, and were placed into a hypoxic jar for 24 h. GS-Rb1 at concentrations from 2.5 to 40 µM was given during hypoxic period for 24 h. NRCMs injury was determined by MTT and lactate dehydrogenase (LDH) leakage assay. Cell apoptosis, ROS accumulation, and mitochondrial membrane potential (MMP) were assessed by flow cytometry. Cytosolic translocation of mitochondrial cytochrome c and Bcl-2 family proteins were determined by Western blot. Caspase-3 and caspase-9 activities were determined by the assay kit.Results. GS-Rb1 significantly reduced cell death and LDH leakage induced by H/I. It also reduced H/I induced NRCMs apoptosis induced by H/I, in accordance with a minimal reactive oxygen species (ROS) burst. Moreover, GS-Rb1 markedly decreased the translocation of cytochrome c from the mitochondria to the cytosol, increased the Bcl-2/ Bax ratio, and preserved mitochondrial transmembrane potential (ΔΨm). Its administration also inhibited activities of caspase-9 and caspase-3.Conclusion. Administration of GS-Rb1 during H/Iin vitrois involved in cardioprotection by inhibiting apoptosis, which may be due to inhibition of the mitochondrial apoptotic pathway.

Delayed cytoprotection induced by hypoxic preconditioning in cultured neonatal rat cardiomyocytes: Role of GRP78

Life Sciences ◽  
2007 ◽  
Vol 81 (13) ◽  
pp. 1042-1049 ◽  
Author(s):  
Yan-Xia Pan ◽  
An-Jing Ren ◽  
Juan Zheng ◽  
Wei-Fang Rong ◽  
Hong Chen ◽  
...  
Keyword(s):  
Hypoxic Preconditioning ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

A cardiac α-actin (ACTC1) p. Gly247Asp mutation inhibits SRF-signaling in vitro in neonatal rat cardiomyocytes

2019 ◽  
Vol 518 (3) ◽  
pp. 500-505 ◽  
Author(s):  
Ashraf Yusuf Rangrez ◽  
Lucia Kilian ◽  
Katharina Stiebeling ◽  
Sven Dittmann ◽  
Eric Schulze-Bahr ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

scholarly journals Safflor yellow A protects neonatal rat cardiomyocytes against anoxia/reoxygenation injury in vitro

2013 ◽  
Vol 34 (4) ◽  
pp. 487-495 ◽  
Author(s):  
Jia-lin Duan ◽  
Jing-wen Wang ◽  
Yue Guan ◽  
Ying Yin ◽  
Guo Wei ◽  
...  
Keyword(s):  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes ◽  
Reoxygenation Injury

scholarly journals miRNA-146a Mimic Inhibits NOX4/P38 Signalling to Ameliorate Mouse Myocardial Ischaemia Reperfusion (I/R) Injury

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Lili Xiao ◽  
Yulei Gu ◽  
Gaofei Ren ◽  
Linlin Chen ◽  
Liming Liu ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Myocardial Ischaemia ◽  
Underlying Mechanism ◽  
Neonatal Rat ◽  
Ischaemia Reperfusion Injury ◽  
Rat Cardiomyocytes ◽  
Ischaemia Reperfusion ◽  
Ros Accumulation

Evidence suggests that miR-146a is implicated in the pathogenesis of cardiovascular diseases; however, the role of miR-146a in myocardial ischaemia reperfusion (I/R) injury is unclear. The aim of this study was to explore the functional role of miR-146a in myocardial ischaemia reperfusion injury and the underlying mechanism. C57BL/6J mice were subjected to 45 min of ischaemia and 1 week of reperfusion to establish a myocardial I/R injury model. A miR-146a mimic (0.5 mg/kg) was administered intravenously at the beginning of the ischaemia process. Neonatal rat cardiomyocytes were also subjected to hypoxia/reperfusion (H/R). Cells were treated with the miR-146a mimic or antagonist. As a result, the miR-146a mimic attenuated H/R-induced cardiomyocyte injury, as evidenced by increased cell viability and reduced lactate dehydrogenase (LDH) levels. In addition, the miR-146a mimic inhibited oxidative stress in cells suffering from H/R injury. Moreover, the miR-146a antagonist exerted adverse effects in vitro. In mice with myocardial I/R injury, the miR-146a mimic preserved cardiac function and reduced the infarction area and fibrosis. Moreover, the miR-146a mimic decreased the inflammatory response and reactive oxygen species (ROS) accumulation in mouse hearts. Mechanistically, we found that miR-146a directly regulated the transcription of NOX4, which subsequently affected P38 signalling in cardiomyocytes. When we knocked down NOX4, the effects of the miR-146a antagonist in worsening the cell condition were counteracted in in vitro experiments. Taken together, the results suggest that miR-146a protects against myocardial ischaemia reperfusion injury by inhibiting NOX4 signalling. The miR-146a mimic may become a potential therapeutic approach for patients with myocardial ischaemia reperfusion.

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