Plasminogen Activator Expression Correlates with Genetic Differences in Vascular RemodelingKorshunov V.A.a · Solomatina M.A.b · Plekhanova O.S.b · Parfyonova Y.V.b · Tkachuk V.A.b,c · Berk B.C.a
aCenter for Cardiovascular Research, Aab Institute of Biomedical Sciences and Department of Medicine, University of Rochester, Rochester, N.Y., USA; bMolecular Endocrinology Laboratory, Institute of Experimental Cardiology, Russian Cardiology Research and Production Center, and cMoscow State University, Moscow, Russia
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Article / Publication Details
Intima-media thickening (IMT) of the carotid artery, a form of vascular remodeling, correlates well with coronary artery disease risk in humans. Vascular remodeling in response to blood flow is a complex process that critically involves altered cell matrix interactions. To gain insight into these events, we performed partial carotid ligation (left carotid (LCA) = low flow and right carotid (RCA) = high flow) in 2 inbred mouse strains: C57Bl/6J (C57) and FVB/NJ (FVB). To evaluate the role of the 2 major matrix-degrading systems, plasminogen activators (PAs) and matrix metalloproteinases (MMPs), we compared the expression of u-PA, t-PA, MMP-2 and MMP-9 in ligated carotids of C57 and FVB mice. The extent of remodeling was greater in response to low LCA than high RCA flow. Despite a similar decrease in LCA flow in both strains, maximal IMT volume was greater in FVB (82 ± 7 × 10–6 µm3) than in C57 (38 ± 4 × 10–6 µm3) after ligation. Among PAs and MMPs, increased expression of t-PA and u-PA correlated with increased IMT (p < 0.0005 and p < 0.001, respectively). MMP-2, MMP-9 and tissue inhibitors of metalloproteinase-2 expression also increased, but did not differ between strains. In summary, flow-induced IMT of the carotid is genetically determined and correlates with t-PA and u-PA expression in 2 inbred mouse strains.
© 2004 S. Karger AG, Basel
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