| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
J. Biol. Chem., Vol. 277, Issue 3, 2353-2359, January 18, 2002
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
From the Departments of In response to vascular injury, smooth muscle
cells migrate from the media into the intima, where they
contribute to the development of neointimal lesions. Increased matrix
metalloproteinase (MMP) expression contributes to the migratory
response of smooth muscle cells by releasing them from their
surrounding extracellular matrix. MMPs may also participate in the
remodeling of extracellular matrix in vascular lesions that could lead
to plaque weakening and subsequent rupture. Neurotrophins and their
receptors, the Trk family of receptor tyrosine kinases, are expressed
in neointimal lesions, where they induce smooth muscle cell migration.
We now report that nerve growth factor (NGF)-induced activation of the
TrkA receptor tyrosine kinase induces MMP-9 expression in both primary cultured rat aortic smooth muscle cells and in a smooth muscle cell
line genetically manipulated to express TrkA. The response to NGF was
specific for MMP-9 expression, as the expression of MMP-2, MMP-3, or
the tissue inhibitor of metalloproteinase-2 was not changed. Activation
of the Shc/mitogen-activated protein kinase pathway mediates the
induction of MMP-9 in response to NGF, as this response is abrogated in
cells expressing a mutant TrkA receptor that does not bind Shc and by
pretreatment of cells with the MEK-1 inhibitor, U0126. Thus, these
results indicate that the neurotrophin/Trk receptor system, by virtue
of its potent chemotactic activity for smooth muscle cells and its
ability to induce MMP-9 expression, is a critical mediator in the
remodeling that occurs in the vascular wall in response to injury.
Nerve Growth Factor Activation of Erk-1 and Erk-2 Induces Matrix
Metalloproteinase-9 Expression in Vascular Smooth Muscle Cells*
§,§¶, and§
Pathology and ¶ Cell
Biology and the § Center of Vascular Biology, Joan and
Sanford I. Weill Medical College of Cornell University,
New York, New York 10021
*
This work was supported by American Heart Association
Grant-in-aid 9501510 (to R. K.) and by National Institutes of
Health Public Service Grants HL58623 (to R. K.), PO1 HL46403 (to
R. K.), and HL40819 (to D. J. F.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed: Dept. of
Pathology, Weill Medical College of Cornell University, 1300 York Ave., New York, NY 10021. Tel.: 212-746-6476; Fax: 212-746-8789;
E-mail: rtkraeme@med.cornell.edu.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
 |
|
  R. Kraemer, P. J. Baker, K. C. Kent, Y. Ye, J. J. Han, R. Tejada, M. Silane, R. Upmacis, R. Deeb, Y. Chen, et al. Decreased Neurotrophin TrkB Receptor Expression Reduces Lesion Size in the Apolipoprotein E-Null Mutant Mouse Circulation, December 6, 2005; 112(23): 3644 - 3653. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 N. S. Haque, J. T. Fallon, J. J. Pan, M. B. Taubman, and P. C. Harpel Chemokine receptor-8 (CCR8) mediates human vascular smooth muscle cell chemotaxis and metalloproteinase-2 secretion Blood, February 15, 2004; 103(4): 1296 - 1304. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. H. Yamani, R. C. Starling, D. J. Cook, E. M. Tuzcu, A. Abdo, P. Paul, K. Powell, N. B. Ratliff, Y. Yu, P. M. McCarthy, et al. Donor Spontaneous Intracerebral Hemorrhage Is Associated With Systemic Activation of Matrix Metalloproteinase-2 and Matrix Metalloproteinase-9 and Subsequent Development of Coronary Vasculopathy in the Heart Transplant Recipient Circulation, October 7, 2003; 108(14): 1724 - 1728. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-M. Yang, Z. Xu, H. Wu, H. Zhu, X. Wu, and W. N. Hait Overexpression of Extracellular Matrix Metalloproteinase Inducer in Multidrug Resistant Cancer Cells Mol. Cancer Res., April 1, 2003; 1(6): 420 - 427. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. J. Gavin, S. E. Crawford, S. T. Shulman, F. L. Garcia, and A. H. Rowley Systemic Arterial Expression of Matrix Metalloproteinases 2 and 9 in Acute Kawasaki Disease Arterioscler. Thromb. Vasc. Biol., April 1, 2003; 23(4): 576 - 581. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. W. Kang, I. J. Cho, C. H. Lee, and S. G. Kim Essential Role of Phosphatidylinositol 3-Kinase-Dependent CCAAT/Enhancer Binding Protein {beta} Activation in the Induction of Glutathione S-Transferase by Oltipraz J Natl Cancer Inst, January 1, 2003; 95(1): 53 - 66. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. G. Park, Y.-S. Kang, Y. H. Ahn, S. H. Lee, K.-R. Kim, K.-W. Kim, G. Y. Koh, Y.-G. Ko, and S. Kim Dose-dependent Biphasic Activity of tRNA Synthetase-associating Factor, p43, in Angiogenesis J. Biol. Chem., November 15, 2002; 277(47): 45243 - 45248. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Emanueli, M. B. Salis, A. Pinna, G. Graiani, L. Manni, and P. Madeddu Nerve Growth Factor Promotes Angiogenesis and Arteriogenesis in Ischemic Hindlimbs Circulation, October 22, 2002; 106(17): 2257 - 2262. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| All ASBMB Journals | Molecular and Cellular Proteomics |
| Journal of Lipid Research | ASBMB Today |
