AJP - Heart AJP: Heart and Circulatory Physiology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol (January 23, 2003). doi:10.1152/ajpheart.00942.2001
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
284/6/H2078    most recent
00942.2001v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zhang, Y.
Right arrow Articles by Simons, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhang, Y.
Right arrow Articles by Simons, M.
Submitted on October 30, 2001
Accepted on January 20, 2003

Syndecan 4 modulates basic fibroblast growth factor (FGF2) signaling in vivo

Yufeng Zhang1, Jianyi Li2, Frank W. Sellke2, and Michael Simons1*

1 Cardiology, Dartmouth Medical School, Lebanon, NH, USA
2 Surgery, Beth Israel Deaconess Med Ctr, Boston, MA, USA

* To whom correspondence should be addressed. E-mail: michael.simons{at}dartmouth.edu.

Syndecan-4 is one of the principal heparan sulfate carrying protein on the cell surface. Unlike other members of syndecan family, syndecan mediates PIP2 dependent PKC-{alpha} activation and overexpression of syndecan-4 in vitro results in enhanced FGF2 signaling. The present study was designed to test functional effect of increased syndecan-4 expression in endothelial cells in transgenic mice. Several transgenic mice lines expressing syndecan-4 cDNA under control of human eNOS promoter were generated. Exogenous syndecan-4 was mainly expressed in the heart, brain, and lungs. In particular, the heart demonstrated the greatest increase in the ratio of transgenic to native syndecan-4 gene expression. Vessels from the eNOS-S4 mice demonstrated more pronounced vasodilation to FGF2 but not to VEGF-A165, SNP and A23187 compared to the wild type mice. In order to elucidate the mechanism of this effect, we measured nitric oxide (NO) release from primary cardiac endothelial cells isolated from transgenic or wild type adult mice. Cells from the eNOS-syndecan 4 transgenic mice had a significant increase in FGF2 and VEGF-A165 -induced NO release compared to endothelial cells from the wild type mice. However, the absolute magnitude of this increase was higher for FGF2 than VEGF-A165. In conclusion, enhanced syndecan 4 expression in mouse cardiac endothelial cells results in preferential augmentation of FGF2 but not VEGF-A165-induced NO release.




This article has been cited by other articles:


Home page
 Eur. J. Cardiothorac. Surg.Home page
M. Boodhwani, P. Voisine, M. Ruel, N. R. Sodha, J. Feng, S.-H. Xu, C. Bianchi, and F. W. Sellke
Comparison of vascular endothelial growth factor and fibroblast growth factor-2 in a swine model of endothelial dysfunction
Eur. J. Cardiothorac. Surg., April 1, 2008; 33(4): 645 - 650.
[Abstract] [Full Text] [PDF]

Home page
 J. Cell Sci.Home page
W. Koh, R. D. Mahan, and G. E. Davis
Cdc42- and Rac1-mediated endothelial lumen formation requires Pak2, Pak4 and Par3, and PKC-dependent signaling
J. Cell Sci., April 1, 2008; 121(7): 989 - 1001.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. GenomicsHome page
A. A. Lanahan, T. W. Chittenden, E. Mulvihill, K. Smith, S. Schwartz, and M. Simons
Synectin-dependent gene expression in endothelial cells
Physiol Genomics, November 21, 2006; 27(3): 380 - 390.
[Abstract] [Full Text] [PDF]

Home page
 Circ. Res.Home page
E. Tkachenko, J. M. Rhodes, and M. Simons
Syndecans: New Kids on the Signaling Block
Circ. Res., March 18, 2005; 96(5): 488 - 500.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 1976 by the American Physiological Society.