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Vol. 40, No. 2, 2003
Issue release date: March–April 2003
Section title: Research Paper
J Vasc Res 2003;40:140–148
(DOI:10.1159/000070711)

Requisite Role of p38 MAPK in Mural Cell Recruitment during Angiogenesis in the Rat Aorta Model

Zhu W.-H. · Han J. · Nicosia R.F.
aDepartment of Pathology, University of Washington, Seattle, Wash., bDepartment of Immunology, IMM-32, The Scripps Research Institute, La Jolla, Calif., and cDivision of Pathology and Laboratory Medicine, VA Puget Sound Health Care System, Seattle, Wash., USA

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Published online: 6/19/2003

Number of Print Pages: 9
Number of Figures: 5
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR

Abstract

During the early stage of angiogenesis, neovascular sprouts are composed primarily of endothelial cells. As they mature, microvessels acquire a coating of mural cells, which are critical for the development and maintenance of a functional vasculature. Though growth factor regulation of mural cell recruitment has been extensively investigated, the intracellular signaling events involved in this process remain poorly understood. Among the intracellular kinases implicated in angiogenesis, the p38 MAPK has been shown to transduce signals critical for vascular remodeling and maturation. The rat aorta model of angiogenesis was used to further investigate the role of this signaling pathway in the recruitment of mural cells during angiogenesis. The p38 MAPK inhibitor SB203580 selectively blocked mural cell recruitment, resulting in the formation of naked endothelial tubes without mural cells. SB203580 inhibited angiopoietin-1-induced mural cell recruitment without influencing angiopoietin-1-stimulated endothelial sprouting. Adenoviral vector-mediated expression of a dominant negative form of p38 MAPK significantly reduced mural cell recruitment, whereas overexpression of a constitutively activated form of MKK6, an upstream activator of p38 MAPK, increased mural cell number. These results indicate that the p38 MAPK signaling pathway plays a critical role in mural cell recruitment during neovascularization and may represent a therapeutic target in angiogenesis-related disorders.


  

Author Contacts

Dr. Roberto F. Nicosia
Division of Pathology and Laboratory Medicine (S-113-Lab)
VA Puget Sound Health Care System, 1660 S. Columbian Way
Seattle, WA 98108 (USA)
Tel. +1 206 764 2284, Fax +1 206 764 2001, E-Mail Roberto.Nicosia@va.med.gov

  

Article Information

Received: September 10, 2002
Accepted after revision: December 12, 2002
Number of Print Pages : 9
Number of Figures : 5, Number of Tables : 0, Number of References : 29

  

Publication Details

Journal of Vascular Research (Incorporating International Journal of Microcirculation)
Founded 1964 as Angiologica by M. Comèl and L. Laszt (1964–1973) continued as Blood Vessels by J.A. Bevan (1974–1991)
Official Journal of the European Society for Microcirculation

Vol. 40, No. 2, Year 2003 (Cover Date: March-April 2003)

Journal Editor: U. Pohl, Munich
ISSN: 1018–1172 (print), 1423–0135 (Online)

For additional information: http://www.karger.com/jvr


Article / Publication Details

First-Page Preview
Abstract of Research Paper

Published online: 6/19/2003

Number of Print Pages: 9
Number of Figures: 5
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR


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