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SENP1通过激活OPTN介导的线粒体自噬促进间充质干细胞分化，以减轻脑出血后的神经功能损伤。

SENP1 facilitates OM-MSC differentiation through activating OPTN-mediated mitophagy to mitigate the neurologic impairment following ICH.

作者信息

He Jun, Peng Jun, Li You, Jiang Junwen, Li Jiameng, Lin Long, Wang Jian, Xia Ying

机构信息

Department of Neurosurgery, Haikou Affiliated Hospital of Central South University Xiangya School of Medicine, Haikou 570208, Hainan Province, P.R. China.

出版信息

iScience. 2024 Apr 30;27(6):109865. doi: 10.1016/j.isci.2024.109865. eCollection 2024 Jun 21.

DOI:10.1016/j.isci.2024.109865
PMID:38770132
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11103578/
Abstract

Previous studies have indicated the neuroprotective effect of olfactory mucosa mesenchymal stem cells (OM-MSCs) on brain injury. Intracerebral hemorrhage (ICH) models were established in rats by injecting autologous blood. SENP1 expression was enhanced in neurons but decreased in astrocytes compared to that in OM-MSCs. Overexpression of SENP1 promoted the proliferation and neuronal differentiation, while inhibiting the astrocytic differentiation of OM-MSCs. Conversely, its knockdown had the opposite effect. Moreover, OM-MSCs reduced neurological dysfunction in rats after ICH, and the neuroprotective effect of OM-MSCs could be further enhanced by SENP1 overexpression. In addition, SENP1 promoted mitophagy, which might be related to SENP1-mediated OPTN deSUMOylation. Furthermore, SENP1 promoted neuronal differentiation of OM-MSCs through mitophagy mediated by OPTN. Similar to SENP1, OPTN transfection further enhanced the remission effect of OM-MSC on ICH rats. SENP1 promoted neuronal differentiation of OM-MSCs through OPTN-mediated mitophagy to improve neurological deficits in ICH rats.

摘要

先前的研究表明，嗅黏膜间充质干细胞（OM-MSCs）对脑损伤具有神经保护作用。通过注射自体血在大鼠中建立脑出血（ICH）模型。与OM-MSCs相比，SENP1在神经元中的表达增强，但在星形胶质细胞中表达降低。SENP1的过表达促进了OM-MSCs的增殖和神经元分化，同时抑制了其星形胶质细胞分化。相反，其敲低则产生相反的效果。此外，OM-MSCs减轻了ICH后大鼠的神经功能障碍，SENP1的过表达可进一步增强OM-MSCs的神经保护作用。此外，SENP1促进了线粒体自噬，这可能与SENP1介导的OPTN去SUMO化有关。此外，SENP1通过OPTN介导的线粒体自噬促进了OM-MSCs的神经元分化。与SENP1相似，OPTN转染进一步增强了OM-MSC对ICH大鼠的缓解作用。SENP1通过OPTN介导的线粒体自噬促进OM-MSCs的神经元分化，以改善ICH大鼠的神经功能缺损。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/cf5c48a559a6/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/cf5c48a559a6/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/b74f84daf9b7/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/d9b3e42c8720/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/4695821a0018/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/e896b3e4281e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/4ebab9e1d690/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/936a2f55ab91/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/d1bb921a3340/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3881/11103578/cf5c48a559a6/gr7.jpg

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本文引用的文献

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SUMOylation of optineurin is critical for inhibiting interferon β production.
IGF2BP2的去SUMO化通过稳定SOX11促进OM-MSC的神经元分化，以改善脑出血后的脑损伤。
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Mitophagy in Brain Injuries: Mechanisms, Roles, and Therapeutic Potential.脑损伤中的线粒体自噬：机制、作用及治疗潜力
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神经束蛋白的 SUMOylation 对于抑制干扰素 β 的产生至关重要。
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