Neural Regeneration Research ›› 2014, Vol. 9 ›› Issue (8): 815-820.doi: 10.4103/1673-5374.131597

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Upregulation of Nogo receptor expression induces apoptosis of retinal ganglion cells in diabetic rats

Xuezheng Liu 1, Zhongfu Zuo 1, Wanpeng Liu 1, Zhiyun Wang 1, Yang Hou 2, Yunjie Fu 1, Yuzhi Han 1   

  1. 1 Department of Anatomy, Liaoning Medical University, Jinzhou, Liaoning Province, China
    2 Scientific Experimental Center, Liaoning Medical University, Jinzhou, Liaoning Province, China
  • Received:2014-03-28 Online:2014-04-25 Published:2014-04-25
  • Contact: Xuezheng Liu, M.D., Department of Anatomy, Liaoning Medical University, Jinzhou 121001, Liaoning Province, China, Liuxuezheng168@vip.sina.com.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 31140072, 81300931; the Liaoning Provincial Department of Science and Technology Project, No. 2011225015; the Natural Science Foundation of Liaoning Province in China, No. 2013022055.

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Abstract:

The Nogo receptor is an essential factor for neuronal apoptosis, but the changes in Nogo receptor expression in the retina and the effects of the Nogo receptor on retinal ganglion cell apoptosis in diabetes mellitus remain unclear. We found that Nogo receptor expression was mainly visible in retinal ganglion cells of a rat model of diabetes mellitus induced by streptozotocin. At 12 weeks after onset of diabetes mellitus, Nogo receptor and Rho kinase expression significantly increased in the retina, and retinal ganglion cell apoptosis was apparent. When RNA interference was used to suppress Nogo receptor expression in rat retina, Rho kinase expression was obviously inhibited, and retinal ganglion cell apoptosis was evidently reduced in rats with diabetes mellitus. These results indicate that upregulation of Nogo receptor expression is an important mechanism of retinal ganglion cell apoptosis in rats with diabetes mellitus.

Key words: nerve regeneration, diabetes mellitus, diabetic retinopathy, visual acuity, retinal ganglion cells, apoptosis, Nogo receptor, Rho kinase, myelin-associated protein, NSFC grant, neural regeneration