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Citations to this article

Peptide growth factors can provoke "fetal" contractile protein gene expression in rat cardiac myocytes.
T G Parker, … , S E Packer, M D Schneider
T G Parker, … , S E Packer, M D Schneider
Published February 1, 1990
Citation Information: J Clin Invest. 1990;85(2):507-514. https://doi.org/10.1172/JCI114466.
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Research Article Article has an altmetric score of 3

Peptide growth factors can provoke "fetal" contractile protein gene expression in rat cardiac myocytes.

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Abstract

Cardiac-specific gene expression is intricately regulated in response to developmental, hormonal, and hemodynamic stimuli. To test whether cardiac muscle might be a target for regulation by peptide growth factors, the effect of three growth factors on the actin and myosin gene families was investigated by Northern blot analysis in cultured neonatal rat cardiac myocytes. Transforming growth factor-beta 1 (TGF beta 1, 1 ng/ml) and basic fibroblast growth factor (FGF, 25 ng/ml) elicited changes corresponding to those induced by hemodynamic load. The "fetal" beta-myosin heavy chain (MHC) was up-regulated about four-fold, whereas the "adult" alpha MHC was inhibited greater than 50-60%; expression of alpha-skeletal actin increased approximately two-fold, with little or no change in alpha-cardiac actin. Thus, peptide growth factors alter the program of differentiated gene expression in cardiac myocytes, and are sufficient to provoke fetal contractile protein gene expression, characteristic of pressure-overload hypertrophy. Acidic FGF (25 ng/ml) produced seven- to eightfold reciprocal changes in MHC expression but, unlike either TGF-beta 1 or basic FGF, inhibited both striated alpha-actin genes by 70-90%. Expression of vascular smooth muscle alpha-actin, the earliest alpha-actin induced during cardiac myogenesis, was increased by all three growth factors. Thus, three alpha-actin genes demonstrate distinct responses to acidic vs. basic FGF.

Authors

T G Parker, S E Packer, M D Schneider

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Total citations by year

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Citations to this article in year 2017 (5)

Title and authors Publication Year
Nonmyocyte ERK1/2 Signaling Contributes to Load-Induced Cardiomyopathy in Marfan Mice
Rosanne Rouf, Elena Gallo MacFarlane, Eiki Takimoto, Rahul Chaudhary, Varun Nagpal, Peter Rainer, Julia G. Bindman, Elizabeth E. Gerber, Djahida Bedja, Christopher Schiefer, Karen Miller, Guangshuo Zhu, Loretha Myers, Nuria Amat-Alarcon, Dong I. Lee, Norimichi Koitabashi, Daniel P. Judge, David A. Kass, Harry C. Dietz, III
JCI Insight 2017
Gene Expression Networks in the Murine Pulmonary Myocardium Provide Insight into the Pathobiology of Atrial Fibrillation
JK Boutilier, RL Taylor, T Mann, E McNamara, GJ Hoffman, J Kenny, RJ Dilley, P Henry, G Morahan, NG Laing, KJ Nowak
G3: Genes|Genomes|Genetics 2017
Cardiomyocyte specific overexpression of a 37 amino acid domain of regulator of G protein signalling 2 inhibits cardiac hypertrophy and improves function in response to pressure overload in mice
KN Lee, X Lu, C Nguyen, Q Feng, P Chidiac
Journal of Molecular and Cellular Cardiology 2017
Acute Heart Failure
W Krüger
Acute Heart Failure 2017
Cardiac actions of fibroblast growth factor 23
C Faul
Bone 2017

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