Literature DB >> 25082750

Unexpected anti-hypertrophic responses to low-level stimulation of protease-activated receptors in adult rat cardiomyocytes.

Anke C Fender1, Goran Pavic, Grant R Drummond, Gregory J Dusting, Rebecca H Ritchie.   

Abstract

Activators of protease-activated receptors PAR-1 and PAR-2 such as thrombin and synthetic hexapeptides promote hypertrophy of isolated neonatal cardiomyocytes at pathological concentrations. Since PAR-activating proteases often show dual actions at low vs. high concentrations, the potential hypertrophic effects of low-level PAR activation were examined. In H9c2 cardiomyoblasts, messenger RNA (mRNA) expression of the hypertrophic marker atrial natriuretic peptide (ANP) was significantly increased only by higher concentrations of thrombin, trypsin or the synthetic PAR-2 agonist SLIGRL. The dual PAR-1/PAR-2 agonist SFLLRN did not influence basal ANP mRNA expression in H9c2 cells. Low concentration of thrombin or trypsin (up to 0.1 U/mL) or of the synthetic ligands SFLLRN and SLIGRL (1 μM); however, all suppressed ANP mRNA expression stimulated by angiotensin II (Ang II). The PAR-1 selective ligand TFLLRN exerted a comparable effect as SFLLRN. In adult rat cardiomyocytes, protein synthesis determined by [(3)H]phenylalanine incorporation was not increased by various PAR agonists at concentrations tenfold lower than conventionally used to study PAR function in vitro (10 μM for SFLLRN or SLIGRL, 0.1 U/mL for thrombin or trypsin). The positive control endothelin-1 (ET-1, 60 nM) however significantly increased protein synthesis in adult rat cardiomyocytes. Addition of low concentrations of PAR agonists to cardiomyocytes treated with ET-1 or Ang II suppressed [(3)H]phenylalanine incorporation induced by the hypertrophic stimuli. The inhibitory effect of SFLLRN effect was partially reversed by the PAR-1 antagonist RWJ56110. These findings suggest that physiological concentrations of PAR activators may suppress hypertrophy, in contrast to the pro-hypertrophic effects evident at high concentrations. PAR-1 and PAR-2 may dynamically control cardiomyocyte growth, with the net effect critically dependent upon local agonist concentrations. The precise significance of proposed concept of bimodal PAR function in cardiomyocytes remains to be defined, particularly in vivo where hemodynamic and other regulatory factors may counteract or mask the direct cellular actions described here.

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Year:  2014        PMID: 25082750     DOI: 10.1007/s00210-014-1026-9

Source DB:  PubMed          Journal:  Naunyn Schmiedebergs Arch Pharmacol        ISSN: 0028-1298            Impact factor:   3.000


  37 in total

Review 1.  Proteinase-activated receptors.

Authors:  S R Macfarlane; M J Seatter; T Kanke; G D Hunter; R Plevin
Journal:  Pharmacol Rev       Date:  2001-06       Impact factor: 25.468

2.  Early induction of matrix metalloproteinase-9 transduces signaling in human heart end stage failure.

Authors:  Karni S Moshal; Neetu Tyagi; Valerie Moss; Brooke Henderson; Mesia Steed; Alexander Ovechkin; Giorgio M Aru; Suresh C Tyagi
Journal:  J Cell Mol Med       Date:  2005 Jul-Sep       Impact factor: 5.310

3.  The protease thrombin is an endogenous mediator of hippocampal neuroprotection against ischemia at low concentrations but causes degeneration at high concentrations.

Authors:  F Striggow; M Riek; J Breder; P Henrich-Noack; K G Reymann; G Reiser
Journal:  Proc Natl Acad Sci U S A       Date:  2000-02-29       Impact factor: 11.205

4.  Concentration-dependent dual effect of thrombin on impaired growth/apoptosis or mitogenesis in tumor cells.

Authors:  J Zain; Y Q Huang; X Feng; M L Nierodzik; J J Li; S Karpatkin
Journal:  Blood       Date:  2000-05-15       Impact factor: 22.113

5.  Thrombin-receptor activation and thrombin-induced brain tolerance.

Authors:  Yajun Jiang; Jimin Wu; Ya Hua; Richard F Keep; Jianming Xiang; Julian T Hoff; Guohua Xi
Journal:  J Cereb Blood Flow Metab       Date:  2002-04       Impact factor: 6.200

6.  Tissue prothrombin. Universal distribution in smooth muscle.

Authors:  R D McBane; R S Miller; N L Hassinger; J H Chesebro; Y Nemerson; W G Owen
Journal:  Arterioscler Thromb Vasc Biol       Date:  1997-11       Impact factor: 8.311

7.  Concentration dependent dual effect of thrombin in endothelial cells via Par-1 and Pi3 Kinase.

Authors:  Jong-Sup Bae; Yong-Ung Kim; Moon-Ki Park; Alireza R Rezaie
Journal:  J Cell Physiol       Date:  2009-06       Impact factor: 6.384

8.  SCH 79797, a selective PAR1 antagonist, limits myocardial ischemia/reperfusion injury in rat hearts.

Authors:  Jennifer L Strande; Anna Hsu; Jidong Su; Xiangping Fu; Garrett J Gross; John E Baker
Journal:  Basic Res Cardiol       Date:  2007-04-30       Impact factor: 17.165

Review 9.  Exploiting cGMP-based therapies for the prevention of left ventricular hypertrophy: NO* and beyond.

Authors:  Rebecca H Ritchie; Jennifer C Irvine; Anke C Rosenkranz; Ruchi Patel; Igor R Wendt; John D Horowitz; Barbara K Kemp-Harper
Journal:  Pharmacol Ther       Date:  2009-08-29       Impact factor: 12.310

10.  Molecular and functional analysis of the human prothrombinase gene (HFGL2) and its role in viral hepatitis.

Authors:  G A Levy; M Liu; J Ding; S Yuwaraj; J Leibowitz; P A Marsden; Q Ning; A Kovalinka; M J Phillips
Journal:  Am J Pathol       Date:  2000-04       Impact factor: 4.307

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