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PPAR-γ agonists induce the expression of VEGF and its receptors in cultured cardiac myofibroblasts

  1. Vishnu Chintalgattua,
  2. Gregory S. Harrisa,
  3. Shaw M. Akulab and
  4. Laxmansa C. Katwaa,*
  1. aDepartment of Physiology, The Brody School of Medicine, East Carolina University Greenville, NC USA
  2. bDepartments of Microbiology and Immunology, The Brody School of Medicine, East Carolina University Greenville, NC USA
  1. *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
  • Received July 21, 2006.
  • Revision received December 18, 2006.
  • Accepted January 4, 2007.

Abstract

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)-γ by its agonists induces VEGF expression while simultaneously decreasing inflammation (NF-κB). Such an increase in myoFb VEGF expression by PPAR-γ agonists may play a role in angiogenesis.

Methods: Rat myoFb were treated with PPAR-γ 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-γ 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-γ agonists increased extracellular VEGF, augmenting tubule formation on a Matrigel. The PPAR-γ activator 15J2 significantly decreased the NF-κB activity in myoFb.

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

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    1. Cardiovasc Res (2007) 74 (1): 140-150. doi: 10.1016/j.cardiores.2007.01.010
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