Different roles of ERK(1/2) and p38 MAPK(alpha/beta) in cellular signaling during cardiomyocyte anoxia preconditioning

Preconditioning (PC) exhibits earlier and delayed protection. But the mechanism of cellular signaling in delayed protection of PC remains unclear. We explored the roles of ERK(1/2) and p38 MAPK(alpha/beta) (p38(alpha/beta)) in delayed protection of anoxia preconditioning (APC). The anoxia/reoxygenat...

Full description

Saved in:
Bibliographic Details
Published inSheng li hsüeh pao Vol. 55; no. 4; p. 454
Main Authors Huang, Yi-Feng, Gong, Kai-Zheng, Zhang, Zhen-Gang
Format Journal Article
LanguageChinese
Published China 25.08.2003
Subjects
Online AccessGet more information

Cover

Loading…
More Information
Summary:Preconditioning (PC) exhibits earlier and delayed protection. But the mechanism of cellular signaling in delayed protection of PC remains unclear. We explored the roles of ERK(1/2) and p38 MAPK(alpha/beta) (p38(alpha/beta)) in delayed protection of anoxia preconditioning (APC). The anoxia/reoxygenation (A/R) injury and APC models were established in cultured neonatal rat cardiomyocytes. An ERK(1/2) inhibitor (PD98059) and a p38(alpha/beta) blocker (SB203580) were applied and their effects on A/R and APC models were observed. The cellular contents of MDA, SOD, cell viability and LDH release was measured at the end of the study. ERK(1/2) and p38 MAPK total activity was measured by in-gel myelin basic protein phosphorylation assay at different points during sustained anoxia. The results obtained are as follows: (1) PD98059 (but not SB203580), administered in preconditioning anoxia phase in APC group, abolished completely the delayed protection of APC; (2) SB203580 administered in sustained anoxia phase in A/R gr
ISSN:0371-0874