Experimental Branch Retinal XXXX Induces Upstream Pericyte Loss and Vascular Destabilization.

@entity227 @entity548 @entity10081 @entity19 @entity2994 @entity4 @entity641 @entity10245 @entity63 @entity6980 @entity38207 @entity519 @entity393
AIMS: Branch @entity2994 (BRVO) leads to @entity6980 and is important cause of @entity227 . Although the vascular morphological changes following experimental @entity2994 have been described in a variety of models using angiography, the underlying cellular events are ill defined. METHODS AND RESULTS: We here show that laser-induced experimental BRVO in @entity19 leads to a wave of TUNEL-positive endothelial cell (EC) apoptosis in the upstream vascular network associated with a transient @entity4 and @entity548 . Subsequently, we observe an induction of EC proliferation within the dilated vein and capillaries, detected by @entity10081 incorporation, and the @entity4 resolves. However, the pericytes of the upstream capillaries are severely reduced, which was associated with continuing EC apoptosis and proliferation. The vascular remodeling was associated with increased expression of @entity641 , @entity38207 , but also @entity10245 expression. Exposure of the experimental animals to @entity519 , when pericyte (PC) dropout had occurred, led to a dramatic increase in endothelial cell proliferation, confirming the vascular instability induced by the experimental BRVO. CONCLUSION: Experimental BRVO leads to acute endothelial cells apoptosis and increased permeability. Subsequently the upstream vascular network remains destabilized, characterized by pericyte dropout, un-physiologically high endothelial cells turnover and sensitivity to @entity519 . These early changes might pave the way for @entity393 and subsequent chronic @entity63 and @entity4 that characterize the late stage disease.
