TRANSFORMING GROWTH FACTOR-BETA(1) POTENTIATED ALPHA(1)-ADRENERGIC AND STRETCH-INDUCED C-FOS MESSENGER-RNA EXPRESSION IN RAT MYOCARDIAL-CELLS

被引：17

作者：

MIKI, N ^{[1
]}

HAMAMORI, Y ^{[1
]}

HIRATA, K ^{[1
]}

SUEMATSU, M ^{[1
]}

KAWASHIMA, S ^{[1
]}

AKITA, H ^{[1
]}

YOKOYAMA, M ^{[1
]}

机构：

[1] KOBE UNIV, SCH MED, DEPT INTERNAL MED 1, CHUO KU, KOBE 650, JAPAN

来源：

CIRCULATION RESEARCH | 1994年 / 75卷 / 01期

关键词：

TRANSFORMING GROWTH FACTOR-BETA(1); C-FOS MESSENGER-RNA EXPRESSION; PROTEIN KINASE C; STRETCH STIMULATION;

D O I：

10.1161/01.RES.75.1.8

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Since transforming growth factor-beta(1) (TGF-beta(1)) has been recently shown to be expressed in the heart by mechanical stretch and ischemic injury, we examined the modulation of c-fos mRNA expression and amino acid uptake by TGF-beta(1) in rat myocardial cells. Pretreatment with TGF-beta(1) potentiated norepinephrine (NE)-induced and stretch-induced (+10% and +20% elongation, for 30 minutes) c-fos mRNA expression by 2.2-fold, whereas TGF-beta(1) alone did not induce c-fos mRNA expression in Northern blot analysis. NE-induced [C-14]phenylalanine uptake was also potentiated with TGF-beta(1) pretreatment. The effect of TGF-beta(1) on the NE action was not blocked by propranolol but by prazosin. The protein kinase C activators (12-O-tetradecanoylphorbol 13-acetate [TPA], phorbol 12,13-dibutyrate, and 1-oleyl-2-acetyl-rac-glycerol) induced c-fos mRNA expression, which was also potentiated by TGF-beta 1. Cycloheximide (protein synthesis inhibitor) could not suppress the TGF-beta(1) actions. In nonmuscle cells, TGF-beta(1) modified neither adrenergic nor TPA-induced c-fos mRNA expression. These data suggested that TGF-beta(1) potentiated the c-fos mRNA expression and amino acid incorporation by modification of the alpha(1)-adrenergic and stretch-activated protein kinase C pathway. This mechanism did not require protein synthesis.

引用

页码：8 / 14

页数：7

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