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Am J Physiol Heart Circ Physiol 293: H2597-H2604, 2007. First published July 27, 2007; doi:10.1152/ajpheart.00299.2007
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Role of {alpha}1beta1-integrin in arterial stiffness and angiotensin-induced arterial wall hypertrophy in mice

Huguette Louis,1,2,3 Augustine Kakou,1,2 Veronique Regnault,2,4 Carlos Labat,1,2 Aude Bressenot,2 Jacqueline Gao-Li,5,6 Humphrey Gardner,7 Simon N. Thornton,1,2 Pascal Challande,6,8 Zhenlin Li,5,6 and Patrick Lacolley1,2

1Institut National de la Santé et de la Recherche Médicale, U684, 2Henri Poincare University, and 4Institut National de la Santé et de la Recherche Médicale, U734, Nancy; 5Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7079 and 6Pierre et Marie Curie University, Paris; 8Centre National de la Recherche Scientifique, Unité Mixte de Recherche 7190, Saint-Cyr l'Ecole, France; 3Centre de Recherche Public-Santé, Laboratory of Cardiovascular Research, Luxembourg; and 7Biogen, Incorporated, Cambridge, Massachusetts

Submitted 9 March 2007 ; accepted in final form 21 July 2007

We examined the arterial phenotype of mice lacking {alpha}1-integrin ({alpha}1–/–) at baseline and after 4 wk of ANG II or norepinephrine (NE) administration. Arterial mechanical properties were determined in the carotid artery (CA). Integrin expression, MAPK kinases, and focal adhesion kinase (FAK) were assessed in the aorta. No change in arterial pressure was observed in {alpha}1–/– mice. Elastic modulus-wall stress curves were similar in {alpha}1–/– and {alpha}1+/+ animals, indicating no change in arterial stiffness. The rupture pressure was lower in {alpha}1–/– mice, demonstrating decreased mechanical strength. Lack of {alpha}1-integrin was accompanied by an increase in beta1-, {alpha}v-, and {alpha}5-integrins but no change in {alpha}2-integrin. ANG II increased medial cross-sectional area of the CA in {alpha}1+/+, but not {alpha}1–/–, mice, whereas equivalent pressor doses of NE did not produce a significant increase in either group. In {alpha}1+/+ mice, ANG II induced {alpha}1-integrin expression and smooth muscle cell (SMC) hypertrophy in the CA in association with increased aortic expression of {alpha}-smooth muscle actin and smooth muscle myosin heavy chain and phosphorylation of ERK1/2, p38 MAPK, and FAK. ANG II did not induce SMC hypertrophy or phosphorylation of p38 MAPK and FAK in {alpha}1–/– mice. A functional anti-{alpha}1-integrin antibody inhibited in vitro the ANG II-induced phosphorylation of FAK and p38 MAPK. In conclusion, {alpha}1–/– mice exhibit a reduced mechanical strength at baseline and a lack of ANG II-induced SMC hypertrophy. These results emphasize the importance of {alpha}1beta1-integrin in p38 MAPK and FAK phosphorylation during vascular hypertrophy in response to ANG II.

arterial mechanical properties; vascular hypertrophy; MAPK kinases; integrin expression; smooth muscle cells


Address for reprint requests and other correspondence: P. Lacolley, Unité INSERM U684, 9 Ave. de la Foret de Haye, BP 184, 54505 Vandoeuvre-les-Nancy, France (e-mail: patrick.lacolley{at}nancy.inserm.fr)




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