Effect of heparin on cardiac hypertrophy mediated by the activity of RhoA/Rho kinase signaling pathway

Acta Anatomica Sinica ›› 2009, Vol. 40 ›› Issue (3) : 480-484.

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Acta Anatomica Sinica ›› 2009, Vol. 40 ›› Issue (3) : 480-484. DOI: 10.3969/j.issn.0529-1356.2009.03.027
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Effect of heparin on cardiac hypertrophy mediated by the activity of RhoA/Rho kinase signaling pathway

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Abstract

Objective Cardiac hypertrophy may be regulated primarily by hypertrophystimulating factors.However,little is known about the cardiac growthinhibitory factors that negatively regulate the formation of cardiac Hypertrophy. Recently,a RhoA/Rho kinase signaling pathway was found to be involved in cardiac hypertrophy.The inositol 1,4,5 trisphosphate receptor(IP-3R)is an intracellular Ca SUP>2+/SUP> release channel and specially inhibited by heparin.Heparin was shown to prevent the growth and proliferation of cardiovascular cells besides its wellcharacterized anticoagulant action. We postulated that activation of IP-3R mediated RhoA/Rho kinase pathway had a potential rote in regulation of cardiomyocyte hypertrophy and heparin may antagonize this signaling pathway. Methods Primary neonatal rat cardiomyocytes were cultured in fetal calf serum. Western blotting and RT-PCR were used to evaluate the protein and gene expression. Results IP-3(10SUP>-7/SUP>mol/L)caused a time-dependent increase in c-fos,c-myc, α-actin and βmajor histocompatibility complex (β-MHC) expression of cardiomyocytes(EM>P/EM>0.05).Stimulation of cardiomyocytes with lP3 revealed a timedependent increase in the expressions of RhoA and Rho kinase gene (EM>P/EM>0.05), and heparin could inhibit the effects above mentioned (EM>P/EM>0.05). Concl

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Inositol 1 / 5-trisphosphate receptor(IP-3R) / RhoA/Rho kinase / Signaling transduction / Cardiac hypertrophy / RT-PCR / Western blotting / Rat

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Effect of heparin on cardiac hypertrophy mediated by the activity of RhoA/Rho kinase signaling pathway[J]. Acta Anatomica Sinica. 2009, 40(3): 480-484 https://doi.org/10.3969/j.issn.0529-1356.2009.03.027

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