IGF-I and bFGF Differentially Influence Atrial Natriuretic Factor andα-smooth Muscle Actin Expression in Cultured Atrial Compared to Ventricular Adult Rat Cardiomyocytes

1997 ◽  
Vol 29 (8) ◽  
pp. 2027-2039 ◽  
Author(s):  
Monika Eppenberger-Eberhardt ◽  
Sigrid Aigner ◽  
Marc Y. Donath ◽  
Vreny Kurer ◽  
Paul Walther ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Atrial Natriuretic Factor ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Natriuretic Factor ◽  
Igf I ◽  
Actin Expression ◽  
Atrial Natriuretic

Reexpression of α-smooth muscle actin isoform in cultured adult rat cardiomyocytes

1990 ◽  
Vol 139 (2) ◽  
pp. 269-278 ◽  
Author(s):  
Monika Eppenberger-Eberhardt ◽  
Ingo Flamme ◽  
Vreni Kurer ◽  
Hans M. Eppenberger
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Actin ◽  
Muscle Actin ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Actin Isoform

Insulin-like growth factor-I stimulates myofibrillar genes and modulates atrial natriuretic factor mRNA in rat heart

1997 ◽  
pp. 309-315 ◽  
Author(s):  
MY Donath ◽  
MA Gosteli-Peter ◽  
C Hauri ◽  
ER Froesch ◽  
J Zapf
Keyword(s):  
Rat Heart ◽  
Atrial Natriuretic Factor ◽  
Gh Treatment ◽  
Natriuretic Factor ◽  
Igf I ◽  
Hypophysectomized Rats ◽  
Actin Expression ◽  
Alpha Actin ◽  
Atrial Natriuretic

We have investigated the effect of a 6-day infusion of recombinant human (rh) IGF-I (0.3-1.0 mg/day) or rhGH (200 mU/day) into normal and hypophysectomized rats on the ventricular expression of myofibrillar genes (alpha- and beta-myosin heavy chain (MHC), skeletal and cardiac alpha-actin) and of atrial natriuretic factor (ANF). In normal rats, beta-MHC was not detectable either before or after IGF-I or GH, but alpha-MHC mRNA increased significantly (twofold) with GH (not statistically significant for IGF-I). In contrast to normal rats, hypophysectomized rats did not express alpha-MHC either before or after IGF-I or GH, but beta-MHC was strongly expressed and significantly stimulated (1.8-fold) by IGF-I (not statistically significantly with GH). Skeletal alpha-actin expression remained unchanged during IGF-I or GH treatment of normal rats, but was enhanced by both IGF-I and GH (2.5- and 2.8-fold respectively) in hypophysectomized rats. Expression of cardiac alpha-actin in normal and hypophysectomized rats was not altered by either treatment. IGF-I and GH decreased ventricular expression of ANF in normal rats by 63% and 45% respectively, but did not influence ANF expression in hypophysectomized rats. Our results show that IGF-I and GH (possibly via IGF-I) stimulate expression of myofibrillar genes and modulate ANF mRNA concentrations in rat heart ventricles in vivo, depending on the hormonal status of the animals. However, neither IGF-I nor GH caused a shift from the beta- to the alpha-MHC isoform in hypophysectomized rats.

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