JIP1 Deficiency Protects Retinal Ganglion Cells From Apoptosis in a Rotenone-Induced Injury Model.

ABSTRACT: Retinal ganglion cells (RGCs) undergo apoptosis after injury. c-Jun N-terminal kinase (JNK)-interacting protein 1 (JIP1) is a scaffold protein that is relevant to JNK activation and a key molecule known to regulate neuronal apoptosis. However, the specific role of JIP1 in the apoptosis of RGCs is currently undefined. Here, we used JIP1 gene knockout (KO) mice to investigate the importance of JIP1-JNK signaling in the apoptosis of RGCs in a rotenone-induced injury model. In adult JIP1 KO mice, the number and electrophysiological functions of RGCs were not different from those of wild-type (WT) mice. Ablation of JIP1 attenuated the activation of JNK and the cleavage of caspase-3 in the retina after rotenone injury and contributed to a lower number of TUNEL-positive RGCs, a greater percentage

SUBMITTER: Liu W 

PROVIDER: S-EPMC6804425 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature