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莲座蛋白（LOTUS）过表达可加速小鼠局灶性脑缺血后的神经元可塑性。

LOTUS overexpression accelerates neuronal plasticity after focal brain ischemia in mice.

作者信息

Takase Hajime, Kurihara Yuji, Yokoyama Taka-Akira, Kawahara Nobutaka, Takei Kohtaro

机构信息

Department of Neurosurgery, Yokohama City University Graduate School of Medicine, Yokohama, Japan.

Molecular Medical Bioscience Laboratory, Department of Medical Life Science, Yokohama City University Graduate School of Medical Life Science, Yokohama, Japan.

出版信息

PLoS One. 2017 Sep 7;12(9):e0184258. doi: 10.1371/journal.pone.0184258. eCollection 2017.

DOI:10.1371/journal.pone.0184258
PMID:28880879
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5589167/
Abstract

Nogo receptor-1 (NgR1) and its ligands inhibit neuronal plasticity and limit functional recovery after brain damage such as ischemic stroke. We have previously shown that lateral olfactory tract usher substance (LOTUS) antagonizes NgR1-mediated signaling. Here, we investigated whether LOTUS enhances neuronal plasticity and functional recovery after brain focal ischemia in adult mice. Focal ischemic infarcts were induced in wild-type and LOTUS-overexpressing transgenic mice via middle cerebral artery occlusion. Endogenous LOTUS expression was increased in brain and cervical spinal cord of the contralateral side of ischemia in the chronic phase after brain ischemia. LOTUS overexpression accelerated midline-crossing axonal sprouting from the contralateral side to the ipsilateral side of ischemia in the medullar reticular formation and gray matter of denervated cervical spinal cord. Importantly, LOTUS overexpression improved neurological score highly correlated with laterality ratio of corticoreticular fibers of the medulla oblongata, indicating that LOTUS overexpression may overcome the inhibitory environment induced by NgR1 signaling for damaged motor pathway reconstruction after ischemic stroke. Thus, our data suggest that LOTUS overexpression accelerates neuronal plasticity in the brainstem and cervical spinal cord after stroke and LOTUS administration is useful for future therapeutic strategies.

摘要

Nogo受体-1（NgR1）及其配体可抑制神经元可塑性，并限制脑损伤（如缺血性中风）后的功能恢复。我们之前已经表明，外侧嗅束引导物质（LOTUS）可拮抗NgR1介导的信号传导。在此，我们研究了LOTUS是否能增强成年小鼠脑局灶性缺血后的神经元可塑性和功能恢复。通过大脑中动脉闭塞在野生型和过表达LOTUS的转基因小鼠中诱导局灶性缺血梗死。脑缺血慢性期，缺血对侧脑和颈脊髓中内源性LOTUS表达增加。LOTUS过表达加速了延髓网状结构和去神经支配颈脊髓灰质中从缺血对侧向同侧的中线交叉轴突发芽。重要的是，LOTUS过表达改善了与延髓皮质网状纤维偏侧比高度相关的神经学评分，表明LOTUS过表达可能克服了由NgR1信号传导诱导的抑制环境，以促进缺血性中风后受损运动通路的重建。因此，我们的数据表明，LOTUS过表达可加速中风后脑干和颈脊髓中的神经元可塑性，并且给予LOTUS对未来的治疗策略有用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/a5f7a686e67b/pone.0184258.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/09401f51d45a/pone.0184258.g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/58713dbf0be5/pone.0184258.g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/239d67187dcd/pone.0184258.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/ee423b6d2ccd/pone.0184258.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/a5f7a686e67b/pone.0184258.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/09401f51d45a/pone.0184258.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/ebfe3a6439a2/pone.0184258.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/58713dbf0be5/pone.0184258.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/d64a746451db/pone.0184258.g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/ee423b6d2ccd/pone.0184258.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed1d/5589167/a5f7a686e67b/pone.0184258.g007.jpg

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Mechanisms of Axonal Damage and Repair after Central Nervous System Injury.
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