Abstract 5553: S100A1 Modulates Endothelial Nitric Oxide Availability by Co-ordinate Regulation of Nitric Oxide Synthase Phosphorylation and Gene Expression of Related Signaling Molecules

TL;DRAbstract

Background: S100A1, a Ca 2+ -sensor protein in endothelial cell, regulates endothelial function. S100A1 knockout mice (KO) are hypertensive with impaired nitric oxide (NO) production and endothelial-dependent vasodilatation. We examine the impact of S100A1 on phosphorylation of Ser 1177 and Thr 495 , positive and negative regulatory residues, respectively, in endothelial nitric oxide synthase (eNOS) and on expression of diverse genes involved in eNOS signaling. Methods and Results: Endothelial cells (EC) were isolated and from pulmonary vasculature of wild-type (WT) and KO mice. WT EC exhibited higher proliferative rates than KO measured by WST-method, and expressed as absorbance/5000 cells/well (0.8923±0.091 vs. 0.268±0.055, p<0.05, n=3) and higher NO production (2214.00±1016.17 vs. 566.75±243.79 nM, p<0.05, n=6). Lower eNOS activity in KO was associated with higher and lower basal phosphorylation at Thr 495 and Ser 1177 , respectively. Bradykinin (100 nM) resulted in rapid (1 m

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