© 2000 American Heart Association, Inc.
Vascular Biology |
Altered Flow–Induced Arterial Remodeling in Vimentin-Deficient Mice
From the Department of Pharmacology and Toxicology and Cardiovascular Research Institute Maastricht (P.M.H.S., H.v.E., G.E.F., J.G.R.D.M.), Universiteit Maastricht, Maastricht, the Netherlands; Institut National de la Santé et de la Recherche Médicale (INSERM) U141 (D.H., C.M.B., B.I.L.), IFR Circulation Lariboisière, Université Paris VII, Paris, France; and Unité de Biologie du Developpement (E.C.-G., F.L.-V.), Institute Pasteur, Paris, France.
Correspondence to Dr J.G.R. De Mey, Department of Pharmacology and Toxicology, Universiteit Maastricht, PO Box 616, 6200 MD Maastricht, Netherlands. E-mail j.demey{at}farmaco.unimaas.nl
Abstract—The endothelial cytoskeleton plays a key role in arterial responses to acute changes in shear stress. We evaluated whether the intermediate filament protein vimentin is involved in the structural responses of arteries to chronic changes in blood flow (BF). In wild-type mice (V+/+) and in vimentin-deficient mice (V-/-), the left common carotid artery (LCA) was ligated near its bifurcation, and 4 weeks later, the structures of the occluded and of the contralateral arteries were evaluated and compared with the structures of arteries from sham-operated mice. Body weight and mean carotid artery BF did not differ between the strains, but LCA and right carotid artery (RCA) diameter (737±14 µm [LCA] and 723±14 µm [RCA] for V-/- versus 808±20 µm [LCA] and 796±20 µm [RCA] for V+/+) and medial cross-sectional area (CSAm) were significantly smaller in V-/- (21±1 and 22±2x103 µm2 for LCA and RCA, respectively) than in V+/+ (28±2 and 28±3x103 µm2 for LCA and RCA, respectively). In V+/+, LCA ligation eliminated BF in the occluded vessel (before ligation, 0.35±0.02 mL/min) and increased BF from 0.34±0.02 to 0.68±0.04 mL/min in the RCA. In V-/-, the BF change in the occluded LCA was comparable (from 0.38±0.05 mL/min to zero-flow rates), but the BF increase in the RCA was less pronounced (from 0.33±0.02 to 0.50±0.05 mL/min). In the occluded LCA of V+/+, arterial diameter was markedly reduced (-162 µm), and CSAm was significantly increased (5x103 µm2), whereas in the high-flow RCA of V+/+, carotid artery diameter and CSAm were not significantly modified. In the occluded LCA of V-/-, arterial diameter was reduced to a lesser extent (-77 µm) and CSAm was increased to a larger extent (10x103 µm2) than in V+/+. In contrast to V+/+, the high-flow RCA of V-/- displayed a significant increase in diameter (52 µm) and a significant increase in CSAm (5x103 µm2). These observations provide the first direct evidence for a role of the cytoskeleton in flow-induced arterial remodeling. Furthermore, they dissociate (1) between acute and chronic arterial responses to altered BF, (2) between alterations of lumen diameter and wall mass during arterial remodeling, and (3) between developmental and imposed flow-induced arterial remodeling.
Key Words: vimentin • arterial remodeling • blood flow • mice • carotid arteries
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