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

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.

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Aldosterone Rapidly Represses Protein Kinase C Activity in Neonatal Rat Cardiomyocytes in Vitro

Endocrinology ◽

10.1210/endo.138.8.5352 ◽

1997 ◽

Vol 138 (8) ◽

pp. 3410-3416 ◽

Cited By ~ 22

Author(s):

Atsuhisa Sato ◽

Jun-Ping Liu ◽

John W. Funder

Keyword(s):

Protein Kinase C ◽

Protein Kinase ◽

Neonatal Rat ◽

Rat Cardiomyocytes ◽

Neonatal Rat Cardiomyocytes ◽

Kinase C ◽

Protein Kinase C Activity

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

Acta Pharmacologica Sinica ◽

10.1038/aps.2012.185 ◽

2013 ◽

Vol 34 (4) ◽

pp. 487-495 ◽

Cited By ~ 21

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

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Beta-1-Adrenergic Receptors Mediate Nrf2-HO-1-HMGB1 Axis Regulation to Attenuate Hypoxia/Reoxygenation-Induced Cardiomyocytes Injury in Vitro

Cellular Physiology and Biochemistry ◽

10.1159/000369736 ◽

2015 ◽

Vol 35 (2) ◽

pp. 767-777 ◽

Cited By ~ 19

Author(s):

Jichun Wang ◽

Xiaorong Hu ◽

Jing Xie ◽

Weipan Xu ◽

Hong Jiang

Keyword(s):

Adrenergic Receptors ◽

Pi3k Inhibitor ◽

Neonatal Rat ◽

Control Group ◽

Rat Cardiomyocytes ◽

Neonatal Rat Cardiomyocytes ◽

Nf Kappab ◽

Cultured Cardiomyocytes ◽

Hypoxia Reoxygenation

Backgroud/Aims: The aim of the study was to evaluate the effects of beta1-adrenergic receptors (β1-ARs) -mediated nuclear factor erythroid 2-related factor 2 (Nrf2)-heme oxygenase-1 (HO-1)-high mobility group box 1 protein (HMGB1) axis regulation in hypoxia/reoxygenation (H/R)-induced neonatal rat cardiomyocytes. Methods: The neonatal cultured cardiomyocytes were concentration-dependently pretreated by dobutamine (DOB), a selective β1-adrenergic receptor agonist, in the absence and/or presence of LY294002 (a phosphatidylinositol 3-kinase (PI3K) inhibitor), SB203580 (a p38mitogen-activated-protein kinase (p38MAPK) inhibitor), Nrf2siRNA and HO-1siRNA, respectively, and then treated by H/R. The effects and mechanisms by which H/R-induced cardiomyocytes injury were evaluated. Results: Significant increase of HO-1 was found in neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Significant change for Nrf2 translocation was also revealed in neonatal cultured cardiomyocytes treated with DOB. Insignificant decreases of NF-kappaB p65 activation and HMGB1 release were observed in H/R-induced neonatal cultured cardiomyocytes treated with DOB, when compared to the control group. Importantly, DOB treatment significantly increased the cell viability and decreased the levels of LDH and MDA in H/R-induced cardiomyocytes injury. However, DOB failed to increase HO-1, inhibit NF-kappaB p65 activation, prevent HMGB1 release and attenuate H/R-induced cardiomyocytes injury when the cultured cardiomyocytes were pretreated by Nrf2siRNA, HO-1siRNA, PI3K inhibitor (LY294002) and p38MAPK inhibitor (SB203580), respectively. Conclusions: β1-ARs-mediated Nrf2-HO-1-HMGB1 axis regulation plays a critical protective role in H/R-induced neonatal rat cardiomyocytes injury in vitro via PI3K/p38MAPK signaling pathway.

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Response of Neonatal Rat Cardiomyocytes to Repetitive Mechanical Stimulation In Vitro

Annals of the New York Academy of Sciences ◽

10.1111/j.1749-6632.1995.tb17403.x ◽

1995 ◽

Vol 752 (1 Cardiac Growt) ◽

pp. 19-29 ◽

Cited By ~ 18

Author(s):

HERMAN H. VANDENBURGH ◽

ROSA SOLERSSI ◽

JANET SHANSKY ◽

JOHN W. ADAMS ◽

SCOTT A. HENDERSON ◽

...

Keyword(s):

Mechanical Stimulation ◽

Neonatal Rat ◽

Rat Cardiomyocytes ◽

Neonatal Rat Cardiomyocytes

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TAFII250, Egr-1, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1999.276.3.h803 ◽

1999 ◽

Vol 276 (3) ◽

pp. H803-H814 ◽

Cited By ~ 4

Author(s):

Nacéra Saadane ◽

Lesley Alpert ◽

Lorraine E. Chalifour

Keyword(s):

Single Injection ◽

Neonatal Rat ◽

Cardiac Damage ◽

Rat Cardiomyocytes ◽

Neonatal Cardiomyocytes ◽

Neonatal Rat Cardiomyocytes ◽

Adult Mice ◽

Factor Ii

Differential display identified that gene fragment HA220 homologous to the transcriptional activator factor II 250 (TAFII250) gene, or CCG1, was increased in hypertrophied rodent heart. To determine whether TAFII250 gene expression is modified after cardiac damage, we measured TAFII250 expression in vivo in mouse hearts after injection of the cardiotoxic agent doxorubicin (DXR) and in vitro in DXR-treated isolated rat neonatal cardiomyocytes. In vivo atrial natriuretic factor (ANF), β-myosin heavy chain (β-MHC), Egr-1, and TAFII250 expression increased with dose and time after a single DXR injection, but only ANF and β-MHC expression were increased after multiple injections. After DXR treatment of neonatal cardiomyocytes we found decreased ANF, α-MHC, Egr-1, and TAFII250 expression. Expression of the TAFII250-regulated genes, the D-type cyclins, was increased after a single injection in adult mice and was decreased in DXR-treated cardiomyocytes. Thus expression of Erg-1, TAFII250, and the D-type cyclins is modulated after cardiotoxic damage in adult and neonatal heart.

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