Alpha1-adrenergic stimulation induced hypertrophy in protein kinase C down-regulated cultured cardiac myocytes.
To examine whether protein kinase C (PKC) activation is essential for the induction of cardiac myocyte hypertrophy caused by alpha1-adrenergic stimulation, we investigated the hypertrophic effect of phenylephrine in PKC down-regulated and non-treated cultured cardiac myocytes obtained from neonatal Sprague-Dawley rat ventricles. The treatment with 10 nmol/L 12-tetra decanoylphorbol-13-acetate (TPA) for more than 2 hours decreased PKC activity by approximately 80% without marked hypertrophy. Phenylephrine increased [14C] phenylalanine (Phe) incorporation in both TPA non-treated and treated cells, 1.54- and 1.71-fold as large as control, respectively. The cell surface area also enlarged in both groups, 1.67- and 1.74-fold, respectively. Thus, phenylephrine induced the similar grade hypertrophy in cultured cardiac myocytes even when PKC was down-regulated. These results suggest that conventional PKC activation may not be essential for mediating myocyte hypertrophy by alpha1-adrenergic stimulation.
Kondo
H
H
First Department of Internal Medicine, Kinki University School of Medicine, Osaka-Sayama, Osaka, Japan.
Horiuchi
M
M
Hama
J
J
Kurroka
A
A
Shimada
S
S
Kamoi
K
K
Yamamoto
Y
Y
Watanabe
M
M
Hidaka
H
H
Katori
R
R
Ishikawa
K
K
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology*; D000818:Animals; D006332:Cardiomegaly / Q000209:etiology; D048429:Cell Size / Q000187:drug effects; D002478:Cells, Cultured; D015536:Down-Regulation; D006984:Hypertrophy; D009206:Myocardium / Q000166:cytology* / Q000201:enzymology*; D010656:Phenylephrine / Q000494:pharmacology*; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D015398:Signal Transduction; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
D000316:Adrenergic alpha-Agonists; D010656:Phenylephrine; D011493:Protein Kinase C; D013755:Tetradecanoylphorbol Acetate