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Open AccessArticle

CELSR1 Promotes Neuroprotection in Cerebral Ischemic Injury Mainly through the Wnt/PKC Signaling Pathway

1
Department of Cell Biology, School of Basic Medical Sciences, Shandong University, Jinan 250012, Shandong, China
2
Key Laboratory for Biotech-Drugs Ministry of Health and Key Laboratory for Rare & Uncommon Diseases of Shandong Province, Shandong Medicinal Biotechnology Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250062, Shandong, China
3
Institute of Basic Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250062, Shandong, China
4
Advanced Medical Research Institute, Shandong University, Jinan 250012, Shandong, China
*
Author to whom correspondence should be addressed.
These authors contributed equally to this work.
Int. J. Mol. Sci. 2020, 21(4), 1267; https://doi.org/10.3390/ijms21041267
Received: 28 December 2019 / Revised: 8 February 2020 / Accepted: 10 February 2020 / Published: 13 February 2020
Cadherin epidermal growth factor (EGF) laminin G (LAG) seven-pass G-type receptor 1 (CELSR1) is a member of a special subgroup of adhesion G protein-coupled receptors. Although Celsr1 has been reported to be a sensitive gene for stroke, the effect of CELSR1 in ischemic stroke is still not known. Here, we investigated the effect of CELSR1 on neuroprotection, neurogenesis and angiogenesis in middle cerebral artery occlusion (MCAO) rats. The mRNA expression of Celsr1 was upregulated in the subventricular zone (SVZ), hippocampus and ischemic penumbra after cerebral ischemic injury. Knocking down the expression of Celsr1 in the SVZ with a lentivirus significantly reduced the proliferation of neuroblasts, the number of CD31-positive cells, motor function and rat survival and increased cell apoptosis and the infarct volume in MCAO rats. In addition, the expression of p-PKC in the SVZ and peri-infarct tissue was downregulated after ischemia/ reperfusion. Meanwhile, in the dentate gyrus of the hippocampus, knocking down the expression of Celsr1 significantly reduced the proliferation of neuroblasts; however, it had no influence on motor function, cell apoptosis or angiogenesis. These data indicate that CELSR1 has a neuroprotective effect on cerebral ischemia injury by reducing cell apoptosis in the peri-infarct cerebral cortex and promoting neurogenesis and angiogenesis, mainly through the Wnt/PKC pathway. View Full-Text
Keywords: CELSR1; neurogenesis; angiogenesis; stroke; Wnt/PKC pathway CELSR1; neurogenesis; angiogenesis; stroke; Wnt/PKC pathway
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Wang, L.-H.; Zhang, G.-L.; Liu, X.-Y.; Peng, A.; Ren, H.-Y.; Huang, S.-H.; Liu, T.; Wang, X.-J. CELSR1 Promotes Neuroprotection in Cerebral Ischemic Injury Mainly through the Wnt/PKC Signaling Pathway. Int. J. Mol. Sci. 2020, 21, 1267.

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