EPOR/CD131-mediated attenuation of rotenone-induced retinal degeneration is associated with upregulation of autophagy genes

Mitochondrial dysfunction is a key driver of neurodegeneration. This study aimed to evaluate the protective potential of EPOR/CD131 (heterodimeric erythropoietin receptor) stimulation in the neurodegeneration caused by rotenone-induced mitochondrial dysfunction. The effects of erythropoietin (EPO) a...

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Bibliographic Details
Published in:	Bulletin of RSMU no. 2022(4)
Main Authors:	Soldatov, VO, Pokrovskiy, MV, Puchenkova, OA, Zhunusov, NS, Krayushkina, AM, Grechina, AV, Soldatova, MO, Lapin, KN, Bushueva, OYu
Format:	Journal Article
Language:	English
Published:	01-08-2022
Online Access:	Get full text
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Summary:	Mitochondrial dysfunction is a key driver of neurodegeneration. This study aimed to evaluate the protective potential of EPOR/CD131 (heterodimeric erythropoietin receptor) stimulation in the neurodegeneration caused by rotenone-induced mitochondrial dysfunction. The effects of erythropoietin (EPO) and an EPO mimetic peptide pHBSP were assessed using in vivo and in vitro models. Single injections of 10 µg/kg EPO or 5 µg/kg pHBSP significantly alleviated the degeneration of ganglion cells of the retina in a rotenone-induced retinopathy in rats (p < 0.05). Consistently, in vitro exposure of rotenone-treated murine primary neuroglial cultures to 500 nM EPO or pHBSP significantly rescued the survival of the cells (p < 0.005). The observed enhancement of LC3A, ATG7, Beclin-1, Parkin and BNIP3 mRNA expression by EPOR/CD131 agonists implicates the autophagy and mitophagy activation as a plausible mitoprotective mechanism.
ISSN:	2500-1094 2542-1204
DOI:	10.24075/brsmu.2022.040