Inhibition of the cyclophilin A-CD147 interaction attenuates right ventricular injury and dysfunction after acute pulmonary embolism in rats.

ABSTRACT: Acute pulmonary embolism (APE)-induced inflammation contributes to cardiomyocyte injury and dysfunction in the right ventricle (RV) of the heart. The interactions of cyclophilin A with its ligand extracellular matrix metalloproteinase inducer (EMMPRIN or CD147) may be involved in this inflammatory process. To this end, here we induced APE by intravenous injections of microspheres in Sprague-Dawley rats. We found that after the APE, cyclophilin A and CD147 levels increased synchronously in RV tissue following APE and peaked at 24 h. The cyclophilin A inhibitor cyclosporine A attenuated the APE-induced cyclophilin A levels, and a monoclonal antibody of CD147 (anti-CD147) abrogated the elevation of CD147 in the RV but not the increase of cyclophilin A. Importantly, treatment with cyclosporine

SUBMITTER: Lu G 

PROVIDER: S-EPMC6078437 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature