HDAC6 inhibition prevents TNF-α-induced caspase 3 activation in lung endothelial cell and maintains cell-cell junctions.

摘要: // Jinyan Yu 1, 2, 3 , Mengshi Ma 2 Zhongsen 1 Jian Fu Department of Respiratory Medicine, The Second Hospital Jilin University, Changchun, Jilin, P.R. China Center for Research on Environmental Disease, College University Kentucky, Lexington, KY, USA Toxicology and Cancer Biology, Correspondence to: Fu, email: jian.fu@uky.edu Ma, mazhongsen2005@163.com Keywords: caspase, endothelial, HDAC6, barrier function, inflammation Received: May 05, 2016      Accepted: June 30, Published: July 13, 2016 ABSTRACT Pro-inflammatory mediators such as TNF-α induce caspase activation in endothelial cells, which leads to degradation cellular proteins, induction apoptotic signaling, cell dysfunction. New therapeutic agents that can inhibit may provide protection against inflammatory injury cells. In the present study, we examined effects selective histone deacetylase 6 (HDAC6) inhibition induced cell-cell junction dysfunction lung We also assessed protective HDAC6 a mouse model endotoxemia. demonstrated or knockdown expression was able prevent cells maintain junctions. Mice pre-treated with inhibitors exhibited decreased endotoxin-induced reduced vascular indicated by retention protein VE-Cadherin level alleviated edema. Collectively, our data suggest is potent strategy