作者: S. Nashine , Y. Liu , B.-J. Kim , A. F. Clark , I.-H. Pang
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摘要: PURPOSE To investigate the role of C/EBP homologous protein (CHOP), a proapoptotic protein, and unfolded response (UPR) marker that is involved in endoplasmic reticulum (ER) stress-mediated apoptosis mouse retinal ganglion cell (RGC) death following ischemia/reperfusion (I/R) injury. METHODS Retinal I/R injury was induced adult C57BL/6J wild-type (WT) CHOP knockout (Chop(-/-)) mice by raising IOP to 120 mm Hg for 60 minutes. Expression other UPR markers studied Western blot immunohistochemistry. counts were performed flat mounts stained with an RGC marker. function evaluated scotopic threshold (STR) electroretinography. RESULTS In WT mice, upregulated 30% I/R-injured eyes compared uninjured 3 days after (P < 0.05). Immunohistochemistry confirmed upregulation specifically RGCs. did not affect baseline density or STR amplitude. Ischemia/reperfusion decreased densities amplitudes both Chop(-/-) mice. However, survival RGCs 48% higher 0.05) than Similarly, significantly at 7, 14, 28 Scotopic 7 those CONCLUSIONS Absence partially protects against loss reduction injury, indicating and, thus, ER stress play important