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MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway

The present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-reg... Full description

Journal Title: Neurochemical Research 2016, Vol.41(10), pp.2627-2635
Main Author: Wang, Peng
Other Authors: Liang, Xinyu , Lu, Yijun , Zhao, Xingjian , Liang, Jia
Format: Electronic Article Electronic Article
Language: English
Subjects:
ID: ISSN: 0364-3190 ; E-ISSN: 1573-6903 ; DOI: 10.1007/s11064-016-1975-0
Link: http://dx.doi.org/10.1007/s11064-016-1975-0
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recordid: springer_jour10.1007/s11064-016-1975-0
title: MicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway
format: Article
creator:
  • Wang, Peng
  • Liang, Xinyu
  • Lu, Yijun
  • Zhao, Xingjian
  • Liang, Jia
subjects:
  • MiR-93
  • Nrf2
  • HO-1
  • Oxidative stress
  • Ischemic stroke
ispartof: Neurochemical Research, 2016, Vol.41(10), pp.2627-2635
description: The present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-regulate the miR-93 level. Our results showed that miR-93 levels in the cerebral cortex of mice increased at 24 and 48 h after reperfusion. Importantly, in vivo study demonstrated that treatment with miR-93 antagomir reduced cerebral infarction volume, neural apoptosis and restored the neurological scores. In vitro study demonstrated that miR-93 antagomir attenuated hydrogen peroxide (H 2 O 2 )-induced injury. Moreover, miR-93 antagomir suppressed oxidative stress in I/R brain and H 2 O 2 treated cortical neurons. Furthermore, we founded that down-regulation of miR-93 increased the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1) and the luciferase reporter assay confirmed that miR-93 directly binds to the predicted 3′-UTR target sites of the nrf2 gene. Finally, we found that knockdown of Nrf2 or HO-1 abolished miR-93 antagomir-induced neuroprotection against oxidative stress in H 2 O 2 treated neuronal cultures. These results suggested that miR-93 antagomir alleviates ischemic injury through the Nrf2/HO-1 antioxidant pathway.
language: eng
source:
identifier: ISSN: 0364-3190 ; E-ISSN: 1573-6903 ; DOI: 10.1007/s11064-016-1975-0
fulltext: fulltext
issn:
  • 1573-6903
  • 15736903
  • 0364-3190
  • 03643190
url: Link


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titleMicroRNA-93 Downregulation Ameliorates Cerebral Ischemic Injury Through the Nrf2/HO-1 Defense Pathway
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subjectMiR-93 ; Nrf2 ; HO-1 ; Oxidative stress ; Ischemic stroke
descriptionThe present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-regulate the miR-93 level. Our results showed that miR-93 levels in the cerebral cortex of mice increased at 24 and 48 h after reperfusion. Importantly, in vivo study demonstrated that treatment with miR-93 antagomir reduced cerebral infarction volume, neural apoptosis and restored the neurological scores. In vitro study demonstrated that miR-93 antagomir attenuated hydrogen peroxide (H 2 O 2 )-induced injury. Moreover, miR-93 antagomir suppressed oxidative stress in I/R brain and H 2 O 2 treated cortical neurons. Furthermore, we founded that down-regulation of miR-93 increased the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1) and the luciferase reporter assay confirmed that miR-93 directly binds to the predicted 3′-UTR target sites of the nrf2 gene. Finally, we found that knockdown of Nrf2 or HO-1 abolished miR-93 antagomir-induced neuroprotection against oxidative stress in H 2 O 2 treated neuronal cultures. These results suggested that miR-93 antagomir alleviates ischemic injury through the Nrf2/HO-1 antioxidant pathway.
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abstractThe present study was designed to evaluate the potential role of miR-93 in cerebral ischemic/reperfusion (I/R) injury in mice. The stroke model was produced in C57BL/6 J mice via middle cerebral artery occlusion (MCAO) for 1 h followed by reperfusion. And miR-93 antagomir was transfected to down-regulate the miR-93 level. Our results showed that miR-93 levels in the cerebral cortex of mice increased at 24 and 48 h after reperfusion. Importantly, in vivo study demonstrated that treatment with miR-93 antagomir reduced cerebral infarction volume, neural apoptosis and restored the neurological scores. In vitro study demonstrated that miR-93 antagomir attenuated hydrogen peroxide (H 2 O 2 )-induced injury. Moreover, miR-93 antagomir suppressed oxidative stress in I/R brain and H 2 O 2 treated cortical neurons. Furthermore, we founded that down-regulation of miR-93 increased the expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1) and the luciferase reporter assay confirmed that miR-93 directly binds to the predicted 3′-UTR target sites of the nrf2 gene. Finally, we found that knockdown of Nrf2 or HO-1 abolished miR-93 antagomir-induced neuroprotection against oxidative stress in H 2 O 2 treated neuronal cultures. These results suggested that miR-93 antagomir alleviates ischemic injury through the Nrf2/HO-1 antioxidant pathway.
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doi10.1007/s11064-016-1975-0
pages2627-2635
date2016-10