Thrombin-induced nitric oxide-cGMP pathway dysfunction is mediated via activation of protease-activated receptor-1.
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Exposure of HUVECs to different concentration of the PAR-1 activating peptide TRAP-1 (1 to 100 µg/ml) over 6 hours leads to reduced expression of (A) eNOS, (B) sGC alpha 1 and (C) sGC beta 1, whereas (D) PDE5 protein expression is increased. (E) Prolonged TRAP-10 exposition over 14 hours leads to cGMP depletion in HUVECs in presence of DETA NONOate (100 µM). Data shown as mean ± SEM (A, B, C, D: n = 6/group; E: n = 9/group). *ppp
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2016-02-29
