XXXX gene deletion mitigates microvascular loss in a model of @entity810 .

@entity8 @entity63 @entity19 @entity1235 @entity810 @entity1011 @entity1611
Microvascular rarefaction following an episode of @entity810 ( @entity810 ) is associated with @entity8 . The mechanisms contributing to microvascular rarefaction are not well-understood, although disruption in local angioregulatory substances is thought to contribute. @entity1235 is an endopeptidase important in modifying the extracellular matrix (ECM) and remodeling the vasculature. We examined the role of @entity1235 gene deletion on microvascular rarefaction in a rodent model of @entity63 @entity810 . @entity1235 -null @entity19 and background control (FVB/NJ) @entity19 were subjected to bilateral renal artery clamping for 20 min followed by reperfusion for 14, 28, or 56 days. Serum @entity1011 level in @entity1235 -null @entity19 24 h after injury [1.4 (SD 0.8) mg/dl] was not significantly different from FVB/NJ @entity19 [1.5 (SD 0.6) mg/dl]. Four weeks after @entity63 , FVB/NJ @entity19 demonstrated a 30-40% loss of microvascular density compared with sham-operated (SO) @entity19 . In contrast, microvascular density was not significantly different in the @entity1235 -null @entity19 at this time following injury compared with SO @entity19 . FVB/NJ @entity19 had a 50% decrease in tissue @entity1611 ( @entity1611 ) 2 wk after @entity63 insult compared with SO @entity19 . A significant difference in @entity1611 was not observed in @entity1235 -null @entity19 compared with SO @entity19 . There was no significant difference in the liberation of angioinhibitory fragments from the ECM between @entity1235 -null @entity19 and FVB/NJ @entity19 following @entity63 . In conclusion, @entity1235 deletion stabilizes microvascular density following @entity63 @entity810 in part by preserving tissue @entity1611 levels.
