Original Article

Upregulation of peroxisome proliferator-activated receptor-γ and NADPH oxidases are involved in restenosis after balloon injury†

  1. Hai-Dong Qin1,
  2. Dan Huang2,
  3. Xiao-Dan Weng3,
  4. Feng Xu4,*

Article first published online: 26 JUN 2009

DOI: 10.1002/jcp.21865

Issue

Journal of Cellular Physiology

Journal of Cellular Physiology

Volume 221, Issue 2, pages 387–393, November 2009

Additional Information

How to Cite

Qin, H.-D., Huang, D., Weng, X.-D. and Xu, F. (2009), Upregulation of peroxisome proliferator-activated receptor-γ and NADPH oxidases are involved in restenosis after balloon injury. Journal of Cellular Physiology, 221: 387–393. doi: 10.1002/jcp.21865

Author Information

  1. 1

    Department of Emergency, Nanjing Medical University, Affiliated Nanjing First Hospital, Jiangsu, China

  2. 2

    Department of Pathology, Cancer Hospital, Fudan University, Shanghai, China

  3. 3

    Department of Cardiology, Affiliated Hospital of Nantong College, Jiangsu, China

  4. 4

    Clinical Medical School, Huashan Hospital, Fudan University, Shanghai, China

*Clinical Medical School, Huashan Hospital, Fudan University, Wulumuqi Road 12#, Shanghai 200040, China.

  1. †

    Hai-Dong Qin and Dan Huang contributed equally to this work.

Publication History

  1. Issue published online: 21 AUG 2009
  2. Article first published online: 26 JUN 2009
  3. Manuscript Accepted: 21 MAY 2009
  4. Manuscript Received: 18 JAN 2009

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Abstract

Restenosis is a major complication of percutaneous transluminal coronary angioplasty (PTCA) and is characterized by increased superoxide formation and accumulation of smooth muscle cells (SMCs). The mechanisms through which peroxisome proliferator-activated receptor-γ (PPAR-γ) modulates the pathological process are incompletely defined. In this study, balloon injury of porcine coronary arteries in vivo and cell scraping model in vitro were used to elucidate the pathway via this molecule. PPAR-γ and NADPH oxidase expression significantly increased both in neointimal hyperplasia after balloon injury or in the cultured SMCs after scraping injury. In vitro, PPAR-γ agonist 15-deoxy-Δ12,14-prostagladlin J2 (15d-PGJ2) decreased cell-scraping-induced superoxide generation through suppression of NADPH oxidase activity via down-regulation of p22phox and gp91phox. Furthermore, 15d-PGJ2 could suppress scraping-stimulated proliferation of SMCs. These data demonstrate that upregulation of PPAR-γ and NADPH oxidases are involved in restenosis and activation of PPAR-γ can inhibit the NADPH oxidase-dependent superoxide generation in SMCs after injury. These findings will provide a new potential drug target for restenosis after balloon injury. J. Cell. Physiol. 221: 387–393, 2009. © 2009 Wiley-Liss, Inc.

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