Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax.
Animals
Apoptosis
/ genetics
Cell Line
Cell Proliferation
/ genetics
Cell Survival
/ genetics
Gene Silencing
Guanine Nucleotide-Releasing Factor 2
/ deficiency
Mitogen-Activated Protein Kinase 1
/ metabolism
Mitogen-Activated Protein Kinase 3
/ metabolism
Myocytes, Cardiac
/ cytology
Phosphoproteins
/ metabolism
Rats
bcl-2-Associated X Protein
/ metabolism
Bax
H9C2 cell line
apoptosis
cardiac myocyte
p-ERK1/2
rap guanine nucleotide exchange factor 1
survival
Journal
Clinical and experimental pharmacology & physiology
ISSN: 1440-1681
Titre abrégé: Clin Exp Pharmacol Physiol
Pays: Australia
ID NLM: 0425076
Informations de publication
Date de publication:
03 2019
03 2019
Historique:
received:
27
03
2018
revised:
23
08
2018
accepted:
23
08
2018
pubmed:
29
8
2018
medline:
21
4
2020
entrez:
29
8
2018
Statut:
ppublish
Résumé
Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro-survival and anti-apoptotic roles through molecule phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p-ERK1/2 and pro-apoptotic molecule Bax. In this study, the rat-derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the cardiomyocytes. Then, contrary experiments were conducted using C3G overexpression. The cell proliferation and apoptosis were analyzed in the cardiomyocytes which were treated with or without hypoxia/reoxygenation (H/R). Silencing of C3G leaded to significant increase in cell survival inhibition and apoptosis, combined with aggravated the injuries induced by H/R. Overexpression of C3G reduced the injuries induced by the silencing of C3G in the cardiomyocytes via regulation of p-ERK1/2 and Bax. In conclusion, our results provide new experimental evidence that silencing of C3G can increase cell survival inhibition and apoptosis in cardiomyocytes via regulation of p-ERK1/2 and Bax.
Identifiants
pubmed: 30152875
doi: 10.1111/1440-1681.13027
doi:
Substances chimiques
Guanine Nucleotide-Releasing Factor 2
0
Phosphoproteins
0
bcl-2-Associated X Protein
0
Mitogen-Activated Protein Kinase 1
EC 2.7.11.24
Mitogen-Activated Protein Kinase 3
EC 2.7.11.24
Banques de données
GENBANK
['NP_005303.2', 'XP_017447591.1', 'XP_017447592.1', 'XP_008759905.2', 'XP_017447593.1', 'XP_017447594.1', 'XP_008759906.2', 'XP_008759907.2', 'XP_017447595.1', 'XP_008759908.2', 'XP_017447596.1', 'XP_017447597.1', 'XP_017447598.1', 'XP_006233964.1', 'XM_017592102.1', 'XM_017592103.1', 'XM_008761683.2', 'XM_017592104.1', 'XM_017592105.1', 'XM_008761684.2', 'XM_008761685.2', 'XM_017592106.1', 'XM_008761686.2', 'XM_017592107.1', 'XM_017592108.1', 'XM_017592109.1', 'XM_006233902.3']
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
237-245Informations de copyright
© 2018 John Wiley & Sons Australia, Ltd.