眼科新进展2017，Vol.37Issue(3)：225-229,5.DOI:10.13389/j.cnki.rao.2017.0057
细胞因子信号转导抑制因子3(SOCS3)对视神经损伤大鼠视网膜神经节细胞存活的影响
Suppressors of cytokine signaling 3 inhibits cell viability of retinal ganglion cells after optic nerve injury
党晓洁 1任梅 1朱江 1许治国1
作者信息
- 1. 710004陕西省西安市,西安交通大学医学院附属广仁医院眼科,西安市第四医院眼科,陕西省眼科诊疗中心
- 折叠
摘要
Abstract
Objective To explore the effect and potential mechanism of suppressors of cytokine signaling 3 (SOCS3) knockout on cell viability and apoptosis of retinal ganglion cells (RGCs) after optic nerve injury.Methods The optic nerve transection was used to construct optic nerve injury model of rats,and RGCs were isolated after optic nerve injury.The experimental animals were divided into optic nerve transection injury (ONT) group and sham-operation (Sham) group.The expression of SOCS3 in RGCs was detected by Western blot and RT-PCR in each group.Subsequently,SOCS3 siRNA was transfected into RGCs of Sham group and ONT group,and the experimental were further subdivided into blank control group,negative control group and SOCS3 silence groups.Cell viability was measured by CCK8 and MTr methods.Apoptosis was detected by Hoechst 33342 staining and flow cytometry.Furthermore,the mTOR siRNA and SOCS3 siRNA were co-transfected into RGCs,and cell viability and apoptosis were detected.Results The expression of SOCS3 was dramatically increased at 3 days after injury in the ONT group when compared with Sham group (P =0.049),and it showed an increased tendency gradually along with the extension of injury time.Compared with the blank control in the ONT group,SOCS3 silence markedly promoted cell viability [(49.47 ± 7.35) ％ vs.(73.24 ± 8.70) ％],reduced cell growth inhibition [(27.25 ±0.75)％ vs.(10.96 ± 1.07)％] and apoptosis [(23.06 ± 1.43)％ vs.(10.65 ± 1.77)％].The result of Hoechst 33342 staining indicated that SOCS3 silence ameliorated the cell apoptosis induced by ONT.In addition,SOCS3 silence significantly improved pS6 expression at 2 weeks after injury,and mTOR and SOCS3 co-silence reduced cell viability,increased cell growth inhibition and apoptosis compared with SOCS3 silence group after injury.Conclusion SOCS3 silence promotes injury-induced cell viability of RGCs and suppresses injury-induced apoptosis of RGCs via up-regulating mTOR activity in the later period of injury.关键词
细胞因子信号转导抑制因子/mTOR/视神经损伤/视网膜神经节细胞/增殖Key words
suppressors of cytokine signaling 3/mammalian target of rapamycin/optic nerve injury/retinal ganglion cells/proliferation分类
医药卫生引用本文复制引用
党晓洁,任梅,朱江,许治国..细胞因子信号转导抑制因子3(SOCS3)对视神经损伤大鼠视网膜神经节细胞存活的影响[J].眼科新进展,2017,37(3):225-229,5.
