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KCa3.1 Inhibition Decreases Integrin/Extracellular Matrix Interaction in Vascular Smooth Muscle

We and others have shown intermediate‐conductance, Ca2+‐activated K+ channel (KCa3.1) activation contributes to vascular smooth muscle cell (VSMC) migration. VSMC migration necessitates dynamic changes in integrin‐ECM interaction, including focal adhesion turnover, though little is known regarding the mechanical properties of the integrin/ECM interaction in VSMC and how it is regulated when cells are stimulated with a pro‐migratory agonist. We tested the hypothesis that KCa3.1 activation alters matrix‐integrin adhesion. We used atomic force microscopy (AFM) to determine the binding properties of fibronectin (FN)/α5β1‐integrin and collagen I/ α1β1‐integrin in mouse aortic VSMC (MAVSMC). Sub‐confluent MAVSCM were serum‐starved overnight and treated with PDGF‐BB (10 ng/ml) with and without the KCa3.1 inhibitor, TRAM‐34 (100 nM). AFM probes with a FN‐ or collagen I‐coated beads were brought into contact with the cell surface for 2 min and the probes subsequently pulled away from the cell surface in the z‐axis. With FN coated‐beads, PDGF‐BB increased total force required to break adhesion of bead with the MAVSMC compared to control (2539 ± 705 vs. 1093 ± 114 pN) indicative of increased adhesion to FN. This increase was inhibited by TRAM‐34 and reduced to control levels (1068 ± 182 pN). With collagen I coated‐beads, PDGF‐BB had no effect on the force required to break adhesion with the MAVSMC compared to control (1036 ± 263 vs. 1207 ± 237 pN), however TRAM‐34 did reduce adhesion to collagen I compared to control (636 ± 142 pN). Thus, KCa3.1 activation stimulates acute integrin/ECM interaction in an integrin and ECM specific manner in response to PDGF‐BB.