© The Rockefeller University Press,
0021-9525/1998//241 $5.00
The Journal of Cell Biology, Volume 143, Number 1,
, 1998 241-252
Modulation of Calcium Current in Arteriolar Smooth Muscle by
vβ3 and
5β1 Integrin Ligands
Xin Wu*,
Jon E. Mogford*,
Steven H. Platts*,
George E. Davis
,
Gerald A. Meininger*, and
Michael J. Davis*
* Microcirculation Research Institute and Departments of Medical Physiology,
Pathology and Laboratory Medicine, Texas A & M University Health Science Center, College Station, Texas 77843-1114
Vasoactive effects of soluble matrix proteins and integrin-binding peptides on arterioles are mediated by
vβ3 and
5β1 integrins. To examine the underlying mechanisms, we measured L-type Ca2+ channel current in arteriolar smooth muscle cells in response to integrin ligands. Whole-cell, inward Ba2+ currents were inhibited after application of soluble cyclic RGD peptide, vitronectin (VN), fibronectin (FN), either of two anti–β3 integrin antibodies, or monovalent β3 antibody. With VN or β3 antibody coated onto microbeads and presented as an insoluble ligand, current was also inhibited. In contrast, beads coated with FN or
5 antibody produced significant enhancement of current after bead attachment. Soluble
5 antibody had no effect on current but blocked the increase in current evoked by FN-coated beads and enhanced current when applied in combination with an appropriate IgG. The data suggest that
vβ3 and
5β1 integrins are differentially linked through intracellular signaling pathways to the L-type Ca2+ channel and thereby alter control of Ca2+ influx in vascular smooth muscle. This would account for the vasoactive effects of integrin ligands on arterioles and provide a potential mechanism for wound recognition during tissue injury.
Key Words: voltage-gated Ca2+ channel vascular smooth muscle wound repair extracellular matrix integrin-mediated signaling
Abbreviations used in this paper: ECM, extracellular matrix; F11, β3 integrin monoclonal antibody; FAK, focal adhesion kinase; FN, fibronectin; HM
5-1,
5 integrin monoclonal antibody; IBa, whole-cell Ba2+ current; MHC, anti–rat IgG monoclonal antibody; PSS, physiological saline solution; SMC, smooth muscle cell(s); VN, vitronectin.
Address all correspondence to Michael J. Davis, Department of Medical Physiology, 336 Reynolds Medical Building, Texas A & M University Health Science Center, College Station, TX 77843-1114. Tel.: (409) 845-7816. Fax: (409) 847-8635. E-mail: mjd{at}tamu.edu

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