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Relationship between vascular smooth muscle cell stiffness and integrin‐mediated collagen adhesion in response to specific vasoconstrictors and vasodilators
Author(s) -
Reeves Kimberley Jayne,
Hong Zhongkui,
Sun Zhe,
Li Zhaohui,
Meininger Gerald Alan
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.679.7
Subject(s) - vascular smooth muscle , adhesion , vasodilation , fibronectin , chemistry , integrin , extracellular matrix , cell adhesion , arteriole , angiotensin ii , medicine , microbiology and biotechnology , endocrinology , cell , microcirculation , biology , biochemistry , smooth muscle , receptor , organic chemistry
Vascular smooth muscle cells (VSMCs) regulate vessel diameter by transferring force to the extracellular matrix and surrounding cells. A previous study demonstrated that integrin‐mediated adhesion to fibronectin (FN) is regulated in parallel with VSMC contractile activation in response to vasodilators and vasoconstrictors. Aim of this study was to determine whether collagen I (CNI) adhesion was also altered in parallel during changes in VSMC contractile activation in response to vasoconstrictors and vasodilators. VSMCs were isolated from the rat cremaster skeletal muscle feed arteriole and maintained in culture for 5–12 days without passage. Adhesion and cell stiffness were measured using atomic force microscopy (AFM). AFM probes with microsphere‐attached tips were functionalized with CNI (1mg\ml). VSMC stiffness and adhesion were assessed by bringing the AFM probe into cyclic contact with the cell membrane (0.1 Hz) before and after treatment (n=10/group) with angiotensin II (ANG; 10 −6 ) or adenosine (ADO; 10 −4 ). Results indicate that ANG increased both VSMC stiffness and CNI adhesion, whereas adenosine decreased VSMC stiffness and adhesion. Results support the hypothesis that integrin adhesion is dynamically up regulated in VSMC during contractile activation and down regulated during relaxation. (1P01HL095486 to G.A.M.)