Abnormal expression of stromelysin-2 (MMP10) in Marfan syndrome (MFS) and bicuspid aortic valve (BAV) aneurysm

Do Hong Lien, Nataatmadja Maria and West Malcolm (2007) Abnormal expression of stromelysin-2 (MMP10) in Marfan syndrome (MFS) and bicuspid aortic valve (BAV) aneurysm. Journal of Molecular And Cellular Cardiology, 42 6 (supplement 1): S232-S232.


Author Do Hong Lien
Nataatmadja Maria
West Malcolm
Title Abnormal expression of stromelysin-2 (MMP10) in Marfan syndrome (MFS) and bicuspid aortic valve (BAV) aneurysm
Journal name Journal of Molecular And Cellular Cardiology   Check publisher's open access policy
ISSN 0022-2828
1095-8584
Publication date 2007-06
Sub-type Other
DOI 10.1016/j.yjmcc.2007.03.699
Volume 42
Issue 6 (supplement 1)
Start page S232
End page S232
Total pages 1
Place of publication London
Publisher Academic Press Ltd Elsevier Science Ltd
Language eng
Subject 11 Medical and Health Sciences
Abstract Matrix metalloproteinases (MMPs) participating in extracellular matrix remodelling and degradation are believed to be important mechanisms in the development of aortic aneurysm. Expression of matrix metalloproteinase-10 (MMP10) leading to the breakdown of protein components associated with cell–cell adhesions and cell–cell matrix attachments may also be a factor resulting in structural disorganization, cell detachment and abnormal cell migration, proliferation and apoptosis. We have examined the distribution and expression of MMP10 in the aortic wall and in cultured vascular smooth muscle cells (VSMCs) of normal aorta and aortic aneurysm associated with MFS and BAV. Aortic tissue was collected from normal (4 M; 9 F; age 40 ± 12 years, mean ± SD), MFS (6 M; 3 F; 42 ± 24 years) and BAV (10 M; 4 F; 62 ± 17 years). Immunohistochemistry of aortic tissue showed enhanced expression of MMP10 in MFS and BAV VSMCs (normal = 2.2 ± 0.3; MFS = 3.0 ± 1.4; BAV = 3.8 ± 1.1, arbitrary units/VSMC/microscope field). Similarly, cultured VSMCs showed increased expression of MMP10 in cultured MFS and BAV aneurysm (moderate) compared to control VSMCs (mild). Scratch wound migration assay revealed MMP10 expression at the leading front of cell migration. Increased expression of MMP10 was also observed in apoptotic VSMCs that were stained positively with cleaved caspase-3. Overexpression of MMP10 in migrating VSMCs derived from MFS and BAV aneurysm suggests abnormal regulation of MMP10 that is likely to contribute to weaker cell and matrix bonding and the progression of aneurysm.
Keyword Cardiac & Cardiovascular Systems
Cell Biology
metalloproteinases
smooth muscle
Q-Index Code CX
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Other
Collections: Excellence in Research Australia (ERA) - Collection
School of Medicine Publications
 
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Created: Mon, 18 Feb 2008, 14:12:24 EST