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  • Title: Basic fibroblast growth factor-induced endothelial proliferation and NO synthesis involves inward rectifier K+ current.
    Author: Scharbrodt W, Kuhlmann CR, Wu Y, Schaefer CA, Most AK, Backenköhler U, Neumann T, Tillmanns H, Waldecker B, Erdogan A, Wiecha J.
    Journal: Arterioscler Thromb Vasc Biol; 2004 Jul; 24(7):1229-33. PubMed ID: 15130912.
    Abstract:
    OBJECTIVE: Inward rectifier K+ currents (K(ir)) determine the resting membrane potential and thereby modulate essential Ca2+-dependent pathways, like cell growth and synthesis of vasoactive agents in endothelial cells. Basic fibroblast growth factor (bFGF) acts as a vasodilatator and angiogenic factor. Therefore, we investigated the effect of bFGF on K(ir) and assessed the role in proliferation and nitric oxide (NO) formation of endothelial cells. METHODS AND RESULTS: Using the patch-clamp technique, we found characteristic K(ir) in human umbilical cord vein endothelial cells (HUVEC), which were dose-dependently blocked by barium (10 to 100 micromol/L). Perfusion with bFGF (50 ng/mL) caused a significant increase of K(ir), which was blocked by 100 micromol/L barium (n=18, P<0.01). The bFGF-induced HUVEC proliferation was significantly inhibited when using 50 to 100 micromol/L barium (n=6; P<0.01). NO production was examined using a cGMP radioimmunoassay. bFGF caused a significant increase of cGMP levels (n=10; P<0.05), which were blocked by barium. CONCLUSIONS: Modulation of K(ir) plays an important role in bFGF-mediated endothelial cell growth and NO formation.
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