miR-29c-5p knockdown reduces inflammation and blood–brain barrier disruption by upregulating LRP6
Abstract: Blood–brain barrier participates in the pathological process of ischemic stroke. MicroRNA-29c-5p was highly expressed in clinical samples from patients with ischemic stroke. In this study, oxygen-glucose deprivation (OGD) treatment of astrocytes enhanced the permeability of brain microvascular endothelial cells (BMECs), and the miR-29c-5p expression was elevated in clinical samples from patients with ischemic stroke. For the function of miR-29c-5p in ischemic stroke, the miR-29c-5p knockdown decreased the permeability and the tight junction protein (TJP) destruction of BMECs and ameliorated the inflammation induced by OGD-treated astrocytes. Mechanistically, miR-29c-5p interacted with lipoprotein receptor-related protein 6 (LRP6) and negatively regulated the LRP6 expression in astrocytes. Moreover, the rescue assays indicated that the interference with miR-29c-5p ameliorated the TJP destruction of BMECs and inflammation caused by OGD-treated astrocytes by increasing the LRP6 expression. Together, miR-29c-5p knockdown decreased the high permeability and the TJP destruction of BMECs and ameliorated the inflammation induced by OGD-treated astrocytes by elevating LRP6 expression.
- Location
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Deutsche Nationalbibliothek Frankfurt am Main
- Extent
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Online-Ressource
- Language
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Englisch
- Bibliographic citation
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miR-29c-5p knockdown reduces inflammation and blood–brain barrier disruption by upregulating LRP6 ; volume:17 ; number:1 ; year:2022 ; pages:353-364 ; extent:12
Open medicine ; 17, Heft 1 (2022), 353-364 (gesamt 12)
- Creator
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Dai, Qijun
Sun, Jian
Dai, Tianyi
Xu, Qin
Ding, Yueqin
- DOI
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10.1515/med-2022-0438
- URN
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urn:nbn:de:101:1-2022071515114326326430
- Rights
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Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
- Last update
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15.08.2025, 7:29 AM CEST
Data provider
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.
Associated
- Dai, Qijun
- Sun, Jian
- Dai, Tianyi
- Xu, Qin
- Ding, Yueqin
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