Medical Journals

Expression and Function of Vascular Endothelial Growth Factor Receptors (Flt-1 and Flk-1) in Vascular Adventitial Fibroblasts.

Authors:
  • Jin Xin
  • Ge Xiaoli
  • Zhu Ding-liang
  • Yan Chen
  • Chu Yu-Feng
  • Chen Wen-dong
  • Liu Jianjun
  • Gao Ping-jin

From: Laboratory of Vascular Biology, Institute of Health Science Center, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.

Journal of molecular and cellular cardiology

  • Publish Date: Sep 2007
  • ISSN: 0022-2828
  • Volume: 43
  • Issue: 3
  • Pages: 292-300
  • Medium: Print
  • Language: English
  • Citation (JAMA): Jin Xin, Ge Xiaoli, Zhu Ding-liang, et al. Expression and Function of Vascular Endothelial Growth Factor Receptors (Flt-1 and Flk-1) in Vascular Adventitial Fibroblasts.. J. Mol. Cell. Cardiol. Sep 2007;43:292-300

Abstract

Vascular endothelial growth factor receptors (VEGFRs) are previously considered to exist exclusively in endothelial cells. However, little is known if the receptors are expressed in other non-endothelial cells. In this study, we measured activation of two VEGFRs, Flk-1 and Flt-1, and their biological functions in cultured adventitial fibroblasts and injured rat carotid injury arteries induced by balloon angioplasty. Our results indicated that Flt-1, but not Flk-1, existed in adventitial fibroblasts. Angiotensin II increased Flt-1 protein expression in a time- and concentration-dependent manner. Adventitial fibroblast migration stimulated by vascular endothelial growth factor (VEGF) and placental growth factor (PIGF) required Flt-1 expression. The Flt-1-induced adventitial fibroblast migration was blocked by anti-Flt-1 neutralizing antibody and soluble VEGFR1 protein (sFlt-1). However, Flt-1 activation did not enhance cell proliferation. In addition, Flt-1 expression was significantly increased in the neointima and adventitia in injured rat carotid arteries. We concluded that functional expression of Flt-1 in adventitial fibroblasts might be an important mediator in the pathogenesis of vascular remodeling after arterial injury.

Mesh Headings (Keywords): Angiotensin II, Animals, Aorta, Thoracic, Arteries, Carotid Arteries, Cell Movement, Cells, Cultured, Connective Tissue, Dose-Response Relationship, Drug, Fibroblasts, Immunohistochemistry, Male, Rats, Rats, Sprague-Dawley, Time Factors, Tunica Intima, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factor Receptor-1, Vascular Endothelial Growth Factor Receptor-2


Check for Full Text / PubMed Unique Identifier (PMID): 17651752


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

Linked medical terms appearing on this page are added by Healia to help readers find more information and are not part of the original PubMed document.

The data herein was last updated on July 8th, 2008 and may not reflect the most current and accurate data available from NLM.


Advertisements

About | Privacy Policy | Business Solutions | Advertise | Contact | Add Healia to your site

©2012. Healia / Meredith Corporation  

Use of this site constitutes acceptance of our Terms of Service and Privacy Policy. All content on this Web site, including medical opinion and any other health-related information, is for informational purposes only and should not be used for a specific diagnosis or individual treatment plan for any situation. Use of this site and the information contained herein does not create a doctor-patient relationship. Always seek the direct advice of your doctor in connection with any questions or issues you may have regarding your own health or the health of others.