Activation of ATF4 triggers trabecular meshwork cell dysfunction and apoptosis in POAG
Ying Ying, Ran Xue, Yangfan Yang, Sarah X. Zhang, Hui Xiao, Huazhang Zhu, Jingming Li, Guo Chen, Yiming Ye, Minbin Yu, Xing Liu, Yimin Zhong
Abstract
study in mice, we showed that overexpression of ATF4 in the TM induced C/EBP homologous protein (CHOP) expression and TM cells apoptosis, contributing to inflammatory cytokine production, and probably IOP elevation. More importantly, upregulation of ATF4 and CHOP, and colocalization of ATF4 with ELAM-1 were found in the TM of POAG patients. These results suggest that ATF4 is a critical mediator of oxidative stress and ER stress-induced TM cell dysfunction and apoptosis in POAG.
Topics & Concepts
Trabecular meshworkATF4ApoptosisMedicineGlaucomaOphthalmologyCancer researchCell biologyBiologyUnfolded protein responseGeneticsEndoplasmic Reticulum Stress and DiseaseAdvanced Glycation End Products researchUbiquitin and proteasome pathways