Open AccessSerine racemase deletion attenuates neurodegeneration and microvascular damage in diabetic retinopathy
Author(s) -
Hironori Ozaki,
Ran Inoue,
Takako Matsushima,
Masakiyo Sasahara,
Atsushi Hayashi,
Hisashi Mori
Publication year - 2018
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0190864
Subject(s) - neurodegeneration , retinal , diabetic retinopathy , excitotoxicity , retina , medicine , endocrinology , diabetes mellitus , chemistry , glutamate receptor , biology , neuroscience , receptor , ophthalmology , disease
Diabetic retinopathy (DR) is a leading cause of blindness. DR is recognized as a microvascular disease and inner retinal neurodegeneration. In the course of retinal neurodegeneration, N -methyl-D-aspartate receptor (NMDAR)-mediated excitotoxicity is involved. Full activation of NMDAR requires binding of agonist glutamate and coagonist glycine or D-serine. D -Serine is produced from L -serine by serine racemase (SRR) and contributes to retinal neurodegeneration in rodent models of DR. However, the involvement of SRR in both neurodegeneration and microvascular damage in DR remains unclear. Here, we established diabetic model of SRR knockout (SRR-KO) and control wild-type (WT) mice by streptozotocin injection. Six months after the onset of diabetes, the number of survived retinal ganglion cells was higher in SRR-KO mice than that of WT mice. The reduction of thickness of inner retinal layer (IRL) was attenuated in SRR-KO mice than that of WT mice. Moreover, the number of damaged acellular capillaries was lower in SRR-KO mice than that of WT mice. Our results suggest the suppression of SRR activity may have protective effects in DR.