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Objective— Ca2+ -activated K+ (KCa ) channels have been proposed to promote mitogenesis in several cell types. Here, we tested whether the intermediate-conductance KCa channel (IKCa1) and the large-conductance KCa channel (BKCa ) contribute to endothelial cell (EC) proliferation and angiogenesis.Material and Results— Function and expression of IKCa1 and BKCa /Slo were investigated by patch-clamp analysis and real-time RT-PCR in human umbilical vein ECs (HUVECs) and in dermal human microvascular ECs 1 (HMEC-1). HMEC-1 expressed IKCa1 and BKCa /Slo , whereas HUVECs expressed IKCa1. A 48-hour exposure to basic fibroblast growth factor (bFGF) augmented IKCa1 current amplitudes and induced a 3-fold increase in IKCa1 mRNA expression in HUVECs and HMEC-1. Vascular endothelial growth factor (VEGF) was also effective in upregulating IKCa1. BKCa /Slo expression and current amplitudes in HMEC-1 were not altered by bFGF. bFGF- and VEGF-induced EC proliferation was suppressed by charybdotoxin, clotrimazole, or the selective IKCa1 blocker 1-[(2-chlorophenyl)diphenylmethyl]-1H -pyrazole (TRAM-34), whereas inhibition of BKCa /Slo by iberiotoxin was ineffective. In the Matrigel plug assay in mice, administration of TRAM-34 for 2 weeks significantly suppressed angiogenesis by ≈85%.Conclusions— bFGF and VEGF upregulate expression of IKCa1 in human ECs. This upregulation of IKCa1 seems to be required for mitogen-induced EC proliferation and angiogenesis in vivo. Selective IKCa1 blocker might be of therapeutic value to prevent tumor angiogenesis.

arteriosclerosis, thrombosis, and vascular biology

Selective Blockade of the Intermediate-Conductance Ca <sup>2+</sup> -Activated K <sup>+</sup> Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo

Selective Blockade of the Intermediate-Conductance Ca 2+ -Activated K + Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo

Selective Blockade of the Intermediate-Conductance Ca ²⁺ -Activated K ⁺ Channel Suppresses Proliferation of Microvascular and Macrovascular Endothelial Cells and Angiogenesis In Vivo