TGFβ mediated transition of corneal fibroblasts from a proinflammatory state to a profibrotic state through modulation of histone acetylation

• DOI: 10.1002/jcp.22110
• Publication Date: 2010-03-15T15:09:11Z
• Authors: Qingjun Zhou; Lingling Yang; Yao Wang; Mingli Qu; Peng Chen; Ye Wang; Lixin Xie; Jing Zhao; Yiqiang Wang
• Keywords: Proinflammatory cytokine; Myofibroblast

Corneal fibroblasts exhibit different phenotypes in phases of corneal wound healing. In the inflammatory phase, cells assume a proinflammatory phenotype and produce large amounts cytokines chemokines, but proliferative remodeling phases, they adapt profibrotic state, differentiate into myofibroblasts increase extracellular matrix protein synthesis, secretion, deposition. present study, molecular mechanisms regulating transition from state to were investigated. treated with TGFbeta, known anti-inflammatory factor healing, absence or presence trichostatin A (TSA), histone deacetylase (HDAC) inhibitor. The results revealed that TGFbeta induced fibroblasts, including increased morphological changes, assembly actin filaments. Meanwhile, gene expressions down-regulated treatment as confirmed by cDNA microarray, real time PCR ELISA. Moreover, TSA reversed TGFbeta-mediated accompanied hyperacetylations. conclusion, suppressed production factors enhanced expression genes dual roles on regulations mediated altered acetylation.