Premium
PACAP Inhibits Oxidative Stress‐Induced Activation of MAP Kinase‐Dependent Apoptotic Pathway in Cultured Cardiomyocytes
Author(s) -
GASZ BALAZS,
RÁCZ BOGLARKA,
RÖTH ERZSEBET,
BORSICZKY BALAZS,
TAMÁS ANDREA,
BORONKAI ARPAD,
GALLYAS FERENC,
TÓTH GABOR,
REGL?DI DORA
Publication year - 2006
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1317.029
Subject(s) - adenylate kinase , apoptosis , oxidative stress , signal transduction , chemistry , kinase , microbiology and biotechnology , protein kinase a , cyclase , pituitary adenylate cyclase activating peptide , antagonist , endocrinology , medicine , biology , receptor , biochemistry , neuropeptide , vasoactive intestinal peptide
The present article investigated the effect of pituitary adenylate cyclase‐activating polypeptide (PACAP) on oxidative stress‐induced apoptosis in neonatal rat cardiomyocytes. Our results show that PACAP decreased the ratio of apoptotic cells following H 2 O 2 treatment. PACAP also diminished the activity of apoptosis signal‐regulating kinase. These effects of PACAP were counteracted by the PACAP antagonist PACAP6‐38. In summary, our results show that PACAP is able to attenuate oxidative stress‐induced cardiomyocyte apoptosis and suggest that its cardioprotective effect is mediated through inhibition of the MAP kinase‐dependent apoptotic pathway.