Epsin15 Homology Domains: Role in the Pathogenesis of Pulmonary Arterial Hypertension.

ABSTRACT: Intersectin-1s (ITSN) deficiency and expression of a biologically active ITSN fragment, result of granzyme B cleavage under inflammatory conditions associated with pulmonary arterial hypertension (PAH), are characteristics of lung tissue of human and animal models of PAH. Recently, we have shown that this ITSN fragment comprising two Epsin15 homology domains (EH_ITSN) triggers endothelial cell (EC) proliferation and the plexiform arteriopathy in PAH. Limited evidence also indicates that the EH domains of endocytic proteins such as ITSN, upregulate compensatory endocytic pathways in cells with impaired vesicular trafficking. Thus, we sought to investigate whether the EH_ITSN may be involved in this compensatory mechanism for improving the EC endocytic dysfunction induced

SUBMITTER: Predescu D 

PROVIDER: S-EPMC6176378 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature