MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion

Endothelial-to-mesenchymal transition (EndoMT) is a common phenomenon in vascular diseases, while the role of endothelial dysfunction in central vascular disease remains to be further investigated. MiR-122 is an inflammation-associated non-coding RNA that participates in multiple human disease, but...

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Main Authors: Yu, Haiyan, Xu, Jinqiu, Zhu, Pengyin, Zhang, Chunyan
Format: Article
Language:English
Published: Penerbit Universiti Kebangsaan Malaysia 2021
Online Access:http://journalarticle.ukm.my/18304/
http://journalarticle.ukm.my/18304/1/15.pdf
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author Yu, Haiyan
Xu, Jinqiu
Zhu, Pengyin
Zhang, Chunyan
author_facet Yu, Haiyan
Xu, Jinqiu
Zhu, Pengyin
Zhang, Chunyan
author_sort Yu, Haiyan
building UKM Institutional Repository
collection Online Access
description Endothelial-to-mesenchymal transition (EndoMT) is a common phenomenon in vascular diseases, while the role of endothelial dysfunction in central vascular disease remains to be further investigated. MiR-122 is an inflammation-associated non-coding RNA that participates in multiple human disease, but whether miR-122 plays as a critical role in EndoMT induced by ischaemic stroke is unknown. Although BAI2 is known as a brain-specific inhibitor protein of angiogenesis, few studies of BAI2 examined EndoMT. This study investigated the mechanism of EndoMT and the miR-122/BAI2 axis in oxygen-glucose deprivation/reperfusion (OGD/R)-mediated EndoMT. A transient middle cerebral artery occlusion (tMCAO) model and OGD/R treatment were used to mimic the ischaemia-reperfusion injury. The colocalization of CD31 and α-SMA was elevated in the peri-infarct area of tMCAO mice. The expression of miR-122 was decreased in the peri-infarct area of tMCAO mice. Downregulation of miR-122, Occludin, and ZO-1 was observed in human brain microvascular endothelial cells (HBMECs) after OGD/R treatment, while α-SMA expression was increased in HBMECs after OGD/R treatment. MiR-122 overexpression reduced the decrease of Occludin and ZO-1 expression and the increase of α-SMA expression induced by OGD/R. MiR-122 negatively regulated BAI2 expression, and OGD/R treatment enhanced BAI2 expression. Knockdown the expression of BAI2 suppressed the decrease of Occludin and ZO-1 expression and the increase of α-SMA expression induced by OGD/R. In conclusion, miR-122 overexpression attenuates OGD/R-mediated EndoMT by targeting BAI2.
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spelling oai:generic.eprints.org:183042022-04-06T06:19:49Z http://journalarticle.ukm.my/18304/ MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion Yu, Haiyan Xu, Jinqiu Zhu, Pengyin Zhang, Chunyan Endothelial-to-mesenchymal transition (EndoMT) is a common phenomenon in vascular diseases, while the role of endothelial dysfunction in central vascular disease remains to be further investigated. MiR-122 is an inflammation-associated non-coding RNA that participates in multiple human disease, but whether miR-122 plays as a critical role in EndoMT induced by ischaemic stroke is unknown. Although BAI2 is known as a brain-specific inhibitor protein of angiogenesis, few studies of BAI2 examined EndoMT. This study investigated the mechanism of EndoMT and the miR-122/BAI2 axis in oxygen-glucose deprivation/reperfusion (OGD/R)-mediated EndoMT. A transient middle cerebral artery occlusion (tMCAO) model and OGD/R treatment were used to mimic the ischaemia-reperfusion injury. The colocalization of CD31 and α-SMA was elevated in the peri-infarct area of tMCAO mice. The expression of miR-122 was decreased in the peri-infarct area of tMCAO mice. Downregulation of miR-122, Occludin, and ZO-1 was observed in human brain microvascular endothelial cells (HBMECs) after OGD/R treatment, while α-SMA expression was increased in HBMECs after OGD/R treatment. MiR-122 overexpression reduced the decrease of Occludin and ZO-1 expression and the increase of α-SMA expression induced by OGD/R. MiR-122 negatively regulated BAI2 expression, and OGD/R treatment enhanced BAI2 expression. Knockdown the expression of BAI2 suppressed the decrease of Occludin and ZO-1 expression and the increase of α-SMA expression induced by OGD/R. In conclusion, miR-122 overexpression attenuates OGD/R-mediated EndoMT by targeting BAI2. Penerbit Universiti Kebangsaan Malaysia 2021-11 Article PeerReviewed application/pdf en http://journalarticle.ukm.my/18304/1/15.pdf Yu, Haiyan and Xu, Jinqiu and Zhu, Pengyin and Zhang, Chunyan (2021) MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion. Sains Malaysiana, 50 (11). pp. 3313-3320. ISSN 0126-6039 https://www.ukm.my/jsm/malay_journals/jilid50bil11_2021/KandunganJilid50Bil11_2021.html
spellingShingle Yu, Haiyan
Xu, Jinqiu
Zhu, Pengyin
Zhang, Chunyan
MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
title MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
title_full MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
title_fullStr MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
title_full_unstemmed MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
title_short MiR-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
title_sort mir-122-5p attenuates endothelial-to-mesenchymal transition induced by oxygen and glucose deprivation/reperfusion
url http://journalarticle.ukm.my/18304/
http://journalarticle.ukm.my/18304/
http://journalarticle.ukm.my/18304/1/15.pdf