Thrombin Has Biphasic Effects on the Nitric Oxide-cGMP Pathway in Endothelial Cells and Contributes to Experimental Pulmonary Hypertension
Figure 7
Chronic thrombin stimulation leads to nitric oxide-cGMP pathway dysfunction in pulmonary endothelial cells.
Thrombin (30 nM) stimulation over 6 hours reduces the expression of (A, E) eNOS, (B, F) sGC alpha 1 and (C, G) sGC beta 1 in pulmonary artery (A–D) and pulmonary microvascular (E–H) endothelial cells, whereas (D, H) PDE5 expression is increased (White bars: control cells; grey bars: with thrombin). (I) Prolonged thrombin exposition over 14 hours leads to cGMP depletion in pulmonary endothelial cells in presence of DETA NONOate (100 µM). Data shown as mean ± SEM (A, B, C, D: n = 6/group; E, F, G, H: n = 12/group; I: n = 5–6). *p<0.05, **p<0.01 vs cells not exposed to thrombin.