CTRP 9 mitigates the apoptosis and unfolded protein response of OGD/R-induced retinal ganglion cells by regulating the AMPK pathway.

Abstract

C1q/TNF-related protein-9 (CTRP9) has been reported to play roles in several types ofretinal diseases. However, therole and thepotential mechanism ofCTRP9 in glaucoma are still incompletely understood. Theexpression ofCTRP9 in OGD/R-induced retinal ganglion cells (RGCs) was detected by quantitative real-time polymerase chain reaction and western blot assay. Cell proliferation was identified by cell counting Kit-8 assay. Flow cytometry, enzyme-linked immunosorbent assay and western blot assay were performed to assess cell apoptosis. Unfolded protein response (UPR), endoplasmic reticulum (ER) stress and theAMPK pathway were evaluated by western blot assay. Thedata showed that theexpression ofCTRP9 was significantly downregulated in OGD/R-induced 661W cells. OGD/R treatment reduced cell viability, promoted cell apoptosis and activated theUPR and ER stress. Theoverexpression ofCTRP9 reversed theeffects ofOGD/R on 661W cell viability, apoptosis, theUPR and ER stress, as well as theAMPK pathway. However, Compound C, an inhibitor ofAMPK signaling, reversed theprotection ofCTRP9 overexpression against injury from OGD/R in 661W cells. In summary, theresults revealed that CTRP9 abated theapoptosis and UPR ofOGD/R-induced RGCs by regulating theAMPK pathway, which may provide apromising target for thetreatment ofglaucoma.