Abstract
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.
Highlights
Traumatic optic neuropathy is a common clinical problem that occurs in 0.5–5% of patients with closed head injury[1]
Previous studies have reported that Akt activation promotes retinal ganglion cells (RGCs) survival after optic nerve injury (ONI) and activation of the ERK signaling pathway leads to RGC protection in glaucomatous eyes[20,21]
Since the insulin receptor is expressed in the retina including RGCs22, in the present study, we examined the effects of ONI on retinal degeneration in neuritin knockout (KO) mice
Summary
Traumatic optic neuropathy is a common clinical problem that occurs in 0.5–5% of patients with closed head injury[1]. Effective treatments are not established, previous studies have shown that neurotrophins, such as brain-derived neurotrophic factor (BDNF), protect RGCs in animal models of optic nerve injury (ONI)[3,4,5]. Exposure of rat cerebellar granule neurons to neuritin markedly induced phosphorylation of Akt, ERK and mammalian target of rapamycin, in part by activating the insulin receptor signaling pathway[19]. Previous studies have reported that Akt activation promotes RGC survival after ONI and activation of the ERK signaling pathway leads to RGC protection in glaucomatous eyes[20,21]. Since the insulin receptor is expressed in the retina including RGCs22, in the present study, we examined the effects of ONI on retinal degeneration in neuritin knockout (KO) mice
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
