J. Cell Biol., Volume 143, Number 1, October 5, 1998 241-252

Modulation of Calcium Current in Arteriolar Smooth Muscle by _v3 and ₅₁ 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 _v3 and ₅₁ 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-₃ integrin antibodies, or monovalent ₃ antibody. With VN or ₃ 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 _v3 and ₅₁ 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.

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