Short-term inhibition of @entity33559 enhances endothelial regeneration after acute XXXX via enhanced recruitment of circulating progenitor cells.

@entity33559 @entity11132 @entity19 @entity1317 @entity1373 @entity9843 @entity9019 @entity12350 @entity432 @entity731 @entity715 @entity130
BACKGROUND: Endothelial injuries regularly occur in @entity731 and during interventional therapies of the @entity432 . Disturbances in the endothelial integrity can lead to insufficient blood supply and bear the risk of @entity715 formation and acute @entity432 . At present, effective therapeutics to restore endothelial integrity are barely available. We analyzed the effect of pharmacological @entity33559 -inhibition by @entity12350 on endogenous progenitor cell-based endothelial regeneration via the SDF-1a/ @entity9843 -axis after acute endothelial damage in a @entity19 model of @entity130 . METHODS AND RESULTS: Induction of a defined endothelial injury was performed in the carotid artery of C57Bl/6 @entity19 which led to a local upregulation of SDF-1a expression. Animals were treated with placebo, @entity12350 or @entity12350 + @entity9019 . Using mass spectrometry we could prove that @entity12350 prevented cleavage of the chemokine SDF-1a. Accordingly, increased SDF-1a concentrations enhanced recruitment of systemically applied and endogenous circulating @entity9843 + progenitor cells to the site of @entity1317 followed by a significantly accelerated reendothelialization as compared to placebo-treated animals. Improved endothelial recovery, as well as recruitment of circulating @entity9843 + progenitor cells (CD133+, @entity11132 +), was reversed by @entity9843 -antagonization through @entity9019 . In addition, short-term @entity12350 treatment did not significantly promote @entity1373 . CONCLUSION: @entity12350 can accelerate endothelial regeneration after acute endothelial injury. @entity33559 inhibitors prevent degradation of the chemokine SDF-1a and thus improve the recruitment of regenerative circulating @entity9843 + progenitor cells which mediate local endothelial cell proliferation without adversely affecting vessel wall architecture.
