Neural Regeneration Research

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Neuronal cell death and regeneration in diseases associated with advanced glycation end-products accumulation

Guzel Bikbova, Toshiyuki Oshitari, Shuichi Yamamoto   

  1. Department of Ophthalmology and Visual Science, Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba, Japan
  • Received:2014-03-19 Online:2014-04-15 Published:2014-04-15
  • Contact: Toshiyuki Oshitari, M.D., Ph.D., Department of Ophthalmology and Visual Science, Chiba University Graduate School of Medicine, Inohana 1-8-1, Chuo-ku, Chiba 260-8670, Chiba, Japan, Tarii@aol.com or oshitari@faculty.chiba-u.jp .
  • Supported by:

    This study is supported by a Grant-in Aid from the Ministry of Education, Science, Sports and Culture of the Japanese Government.

Abstract:

Growing evidence indicates that neuronal abnormalities including neuronal cell death are associated with the pathogenesis of early diabetic retinopathy. Our previous study of human retinas indicate that mitochondrial and caspase-dependent cell death pathways are associated with retinal neuronal cell degeneration in patients with diabetes Prof. Toshiyuki Oshitari from Chiba University Graduate School of Medicine in Japan had studied and showed a survival effect on damaged retinal neurons induced by diabetic stress. They also found that NT-4 had the best neuroprotective and regenerative effect under high glucose conditions. Earlier study indicated that the maximum rescue ratio of caspase-1, -3, -8, and -9 inhibitors in cultured retinas was 60% in damaged retinal ganglion cells (RGCs). Thus, at least 40% of neuronal cell death in damaged RGCs in cultured retinas should be related to caspase-independent cell death mechanisms. However, no reports have focused on caspase-independent cell death pathways under diabetic stress including AGEs exposure.