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Hydrogen sulfide (H 2 S) is now considered as the third gaseotransmitter, however, the signaling pathways that modulate the biomedical effect of H 2 S on endothelial cells are poorly defined. In the present study, we found in human endothelial cells that H 2 S increased cell migration rates and induced a marked reorganization of the actin cytoskeleton, which was prevented by depletion of Rac1. Pharmacologic inhibiting vascular endothelial growth factor receptor (VEGFR) and phosphoinositide 3-kinase (PI3K) both blunted the activation of Rac1 and the promotion of cell migration induced by H 2 S. Moreover, H 2 S-induced Rac1 activation was selectively dependent on the presence of the PI3K p110α isoform. Activated Rac1 by H 2 S thus in turn resulted in the phosphorylation of the F-actin polymerization modulator, cofilin. Additionally, inhibiting of extracellular signal-regulated kinase (ERK) decreased the augmented cell migration rate by H 2 S, but had no effect on Rac1 activation. These results indicate that Rac1 conveys the H 2 S signal to microfilaments inducing rearrangements of actin cytoskeleton that regulates cell migration. VEGFR-PI3K was found to be upstream pathway of Rac1, while cofilin acted as a downstream effector of Rac1. ERK was also shown to be involved in the action of H 2 S on endothelial cell migration, but independently of Rac1.

PI3K p110α Isoform-Dependent Rho GTPase Rac1 Activation Mediates H2S-Promoted Endothelial Cell Migration via Actin Cytoskeleton Reorganization