XXXX Attenuates Pulmonary Vascular Remodeling in Experimental Pulmonary Arterial Hypertension through Interplay between Endothelial Progenitor Cells and Heme Oxygenase.

@entity455 @entity71267 @entity120 @entity5301 @entity22456 @entity6980 @entity358 @entity35
BACKGROUND: @entity120 ( @entity120 ) is a @entity358 with a high mortality, characterized by typical angio-proliferative lesions. @entity5301 ( @entity5301 ) attenuates @entity6980 in @entity120 . We postulated that @entity5301 acts through mobilization of endothelial progenitor cells (EPCs) and activation of the cytoprotective enzyme @entity22456 (HO-1). METHODS: @entity35 with flow-associated @entity120 , resembling pediatric @entity120 , were treated with HO-1 inducer @entity5301 in the presence or absence of the selective HO-activity inhibitor @entity71267 (SnMP). HO activity, circulating EPCs and @entity455 were assessed after 3   weeks. RESULTS: In @entity120 @entity35 , circulating EPCs were decreased and HO activity was increased compared to control. @entity5301 treatment restored circulating EPCs and improved @entity6980 , as shown by a reduced wall thickness and occlusion rate of the intra-acinar vessels. Inhibition of HO activity with SnMP aggravated @entity120 . Moreover, SnMP treatment abrogated @entity5301 -induced amelioration of @entity6980 , while surprisingly further increasing circulating EPCs as compared with @entity5301 alone. CONCLUSION: In experimental @entity120 , @entity5301 treatment restored the number of circulating EPCs to control level, improved @entity6980 , and showed important interplay with HO activity. Inhibition of increased HO activity in @entity120 @entity35 exacerbated progression of @entity6980 , despite the presence of restored number of circulating EPCs. We suggest that both @entity5301 -induced HO-1 and EPCs are promising targets to ameliorate the pulmonary vasculature in @entity120 .
