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Cardiovascular Research 2007 74(1):140-150; doi:10.1016/j.cardiores.2007.01.010
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Copyright © 2007, European Society of Cardiology

PPAR-{gamma} agonists induce the expression of VEGF and its receptors in cultured cardiac myofibroblasts

Vishnu Chintalgattua, Gregory S. Harrisa, Shaw M. Akulab and Laxmansa C. Katwaa,*

aDepartment of Physiology, The Brody School of Medicine, East Carolina University Greenville, NC USA
bDepartments of Microbiology and Immunology, The Brody School of Medicine, East Carolina University Greenville, NC USA

* Corresponding author. Department of Physiology, Rm. 6E-73C Brody School of Medicine, 600 Moye Blvd. Greenville, NC 27834 USA. Tel.: +1 252 744 1906; fax: +1 252 744 3460. Email address: KatwaL{at}ecu.edu

Objectives: Myofibroblasts (myoFb) are the major cell types that appear at the site of myocardial infarction (MI) in response to injury and play a vital role in tissue repair/remodeling. Since vascular endothelial growth factor (VEGF) plays a crucial role in the infarcted/ischemic heart, we hypothesized that activation of the peroxisome proliferator-activated receptor (PPAR)-{gamma} by its agonists induces VEGF expression while simultaneously decreasing inflammation (NF-{kappa}B). Such an increase in myoFb VEGF expression by PPAR-{gamma} agonists may play a role in angiogenesis.

Methods: Rat myoFb were treated with PPAR-{gamma} agonists and VEGF expression was measured by ELISA. The effect of these agonists on VEGF receptors was determined by qRT-PCR and flow-cytometric analysis. VEGF produced by these cells was also used for analysis of in vitro tubule formation (Matrigel assay).

Results: The PPAR-{gamma} activators troglitazone (TZ) and 15-deoxy-prostaglandin J2 (15J2) induced the expression of VEGF and its receptors (Flt-1 and KDR) in myoFb. TZ and 15J2 elicited a significant increase in the expression of KDR (14.7±1.0% and 9.6±2.1% respectively) and Flt-1 (24.5±2.0%, and 14.0±2.2% respectively) when compared to untreated myoFb. MyoFb treated with PPAR-{gamma} agonists increased extracellular VEGF, augmenting tubule formation on a Matrigel. The PPAR-{gamma} activator 15J2 significantly decreased the NF-{kappa}B activity in myoFb.

Conclusion: This study demonstrates the induction of the VEGF accompanied by a reduction of NF-{kappa}B activity (inflammatory signaling) by PPAR-{gamma} agonists in cardiac myoFb. These results may further the understanding of the beneficial effects of PPAR-{gamma} agonists on infarcted tissue repair and angiogenesis.

KEYWORDS Cardiac myofibroblasts; VEGF; PPAR-{gamma} agonists; Myocardial infarction

Time primary review 28 days


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