Involvement of vascular peroxidase 1 in angiotensin II-induced vascular smooth muscle cell proliferation

Cardiovasc Res. 2011 Jul 1;91(1):27-36. doi: 10.1093/cvr/cvr042. Epub 2011 Feb 3.

Abstract

Aims: Vascular peroxidase 1 (VPO1) is a newly identified haem-containing peroxidase that catalyses the oxidation of a variety of substrates by hydrogen peroxide (H(2)O(2)). Considering the well-defined effects of H(2)O(2) on the vascular remodelling during hypertension, and that VPO1 can utilize H(2)O(2) generated from co-expressed NADPH oxidases to catalyse peroxidative reactions, the aims of this study were to determine the potential role of VPO1 in vascular remodelling during hypertension.

Methods and results: The vascular morphology and the expression of VPO1 in arterial tissues of spontaneously hypertensive rats and Wistar-Kyoto rats were assessed. The VPO1 expression was significantly increased concomitantly with definite vascular remodelling assessed by evaluating the media thickness, lumen diameter, media thickness-to-lumen diameter ratio and mean nuclear area in artery media in spontaneously hypertensive rats. In addition, in cultured rat aortic smooth muscle cells we found that the angiotensin II-mediated cell proliferation was inhibited by knockdown of VPO1 using small hairpin RNA. Moreover, the NADPH oxidase inhibitor, apocynin, and the hydrogen peroxide scavenger, catalase, but not the ERK1/2 inhibitor, PD98059, attenuated angiotensin II-mediated up-regulation of VPO1 and generation of hypochlorous acid.

Conclusion: VPO1 is a novel regulator of vascular smooth muscle cell proliferation via NADPH oxidase-H(2)O(2)-VPO1-hypochlorous acid-ERK1/2 pathways, which may contribute to vascular remodelling in hypertension.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Angiotensin II / metabolism*
  • Animals
  • Aorta, Thoracic / enzymology
  • Aorta, Thoracic / pathology
  • Cell Proliferation* / drug effects
  • Cells, Cultured
  • Disease Models, Animal
  • Enzyme Activation
  • Enzyme Inhibitors / pharmacology
  • Extracellular Matrix Proteins / genetics
  • Extracellular Matrix Proteins / metabolism*
  • Free Radical Scavengers / pharmacology
  • Hydrogen Peroxide / metabolism
  • Hypertension / enzymology*
  • Hypertension / pathology
  • Hypochlorous Acid / metabolism
  • Male
  • Mesenteric Arteries / enzymology
  • Mesenteric Arteries / pathology
  • Mitogen-Activated Protein Kinase 1 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 1 / metabolism
  • Mitogen-Activated Protein Kinase 3 / antagonists & inhibitors
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / enzymology*
  • Muscle, Smooth, Vascular / pathology
  • Myocytes, Smooth Muscle / drug effects
  • Myocytes, Smooth Muscle / enzymology*
  • Myocytes, Smooth Muscle / pathology
  • NADPH Oxidases / antagonists & inhibitors
  • NADPH Oxidases / metabolism
  • Peroxidase / genetics
  • Peroxidase / metabolism*
  • Peroxidasin
  • RNA Interference
  • RNA, Messenger / metabolism
  • Rats
  • Rats, Inbred SHR
  • Rats, Inbred WKY
  • Signal Transduction
  • Time Factors

Substances

  • Enzyme Inhibitors
  • Extracellular Matrix Proteins
  • Free Radical Scavengers
  • RNA, Messenger
  • Angiotensin II
  • Hypochlorous Acid
  • Hydrogen Peroxide
  • Peroxidase
  • NADPH Oxidases
  • Mitogen-Activated Protein Kinase 1
  • Mitogen-Activated Protein Kinase 3