Role of neuritin in retinal ganglion cell death in adult mice following optic nerve injury

• Published in: Scientific reports Vol. 8; no. 1; pp. 10132 - 8
• Main Authors: Azuchi, Yuriko, Namekata, Kazuhiko, Shimada, Tadayuki, Guo, Xiaoli, Kimura, Atsuko, Harada, Chikako, Saito, Atsuko, Yamagata, Kanato, Harada, Takayuki
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 04.07.2018; Nature Publishing Group
• Subjects: 38; 59; 631/378/1686; 631/378/1934; 64/110; 82/51; AKT protein; Cell death; Cell survival; Developmental plasticity; Humanities and Social Sciences; mRNA; multidisciplinary; Neural plasticity; Neuroprotection; Optic nerve; Phosphorylation; Retina; Retinal degeneration; Retinal ganglion cells; Rodents; Science; Science (multidisciplinary); Synaptic plasticity; Synaptogenesis
• ISSN: 2045-2322; 2045-2322
• DOI: 10.1038/s41598-018-28425-7

Neuritin is a small extracellular protein that plays important roles in the process of neural development, synaptic plasticity, and neural cell survival. Here we investigated the function of neuritin in a mouse model of optic nerve injury (ONI). ONI induced upregulation of neuritin mRNA in the retina of WT mice. The retinal structure and the number of retinal ganglion cells (RGCs) were normal in adult neuritin knockout (KO) mice. In vivo retinal imaging and histopathological analyses demonstrated that RGC death and inner retinal degeneration following ONI were more severe in neuritin KO mice. Immunoblot analyses revealed that ONI-induced phosphorylation of Akt and ERK were suppressed in neuritin KO mice. Our findings suggest that neuritin has neuroprotective effects following ONI and may be useful for treatment of posttraumatic complication.