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MicroRNA-98-5p ameliorates oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury by inhibiting Bach1 and promoting Nrf2/ARE signaling.
Biochem Biophys Res Commun. 2018 12 09; 507(1-4):114-121.BB

Abstract

MicroRNA-98-5p (miR-98-5p) is a stress-related microRNA (miRNA) that plays an important role in regulating cell survival, apoptosis, and oxidative stress in multiple cell types and diseases. However, little is known about the role of miR-98-5p in cerebral ischemia/reperfusion injury. In this study, we investigated the role and mechanism of miR-98-5p in regulating neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R), an in vitro model of cerebral ischemia/reperfusion injury. We found that miR-98 expression was significantly altered in neurons in response to OGD/R treatment. Functional experiments showed that overexpression of miR-98-5p inhibited OGD/R-induced apoptosis and reactive oxygen species (ROS) production in neurons, whereas inhibition of miR-98-5p showed the opposite effect. Interestingly, bioinformatics analysis predicted that BTB and CNC homology 1 (Bach1) was a potential target gene of miR-98-5p, that was verified by dual-luciferase reporter assay. Moreover, overexpression of miR-98-5p inhibited Bach1 expression while suppression of miR-98-5p promoted Bach1 expression in neurons. Notably, miR-98-5p was shown to regulate the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and the activity of the antioxidant response element (ARE). However, overexpression of Bach1 or silencing of Nrf2 significantly abolished the miR-98-5p-mediated neuroprotective effect. Overall, these results demonstrate that miR-98-5p ameliorates OGD/R-induced neuronal injury in vitro through targeting to promote activation of Nrf2/ARE signaling. Our study suggests that miR-98-5p may play a potential role in cerebral ischemia/reperfusion injury and represents a potential therapeutic target for neuroprotection.

Authors+Show Affiliations

Department of Neurology, Xi'an No. 4 Hospital, Xi'an, 710004, China.Department of Neurology, Xi'an No. 4 Hospital, Xi'an, 710004, China.Department of Neurology, Xi'an No. 4 Hospital, Xi'an, 710004, China.Department of Neurology, Xi'an No. 4 Hospital, Xi'an, 710004, China.Department of Neurology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710003, China. Electronic address: li_yanlingyl@163.com.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

30449595

Citation

Sun, Xiuyan, et al. "MicroRNA-98-5p Ameliorates Oxygen-glucose Deprivation/reoxygenation (OGD/R)-induced Neuronal Injury By Inhibiting Bach1 and Promoting Nrf2/ARE Signaling." Biochemical and Biophysical Research Communications, vol. 507, no. 1-4, 2018, pp. 114-121.
Sun X, Li X, Ma S, et al. MicroRNA-98-5p ameliorates oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury by inhibiting Bach1 and promoting Nrf2/ARE signaling. Biochem Biophys Res Commun. 2018;507(1-4):114-121.
Sun, X., Li, X., Ma, S., Guo, Y., & Li, Y. (2018). MicroRNA-98-5p ameliorates oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury by inhibiting Bach1 and promoting Nrf2/ARE signaling. Biochemical and Biophysical Research Communications, 507(1-4), 114-121. https://doi.org/10.1016/j.bbrc.2018.10.182
Sun X, et al. MicroRNA-98-5p Ameliorates Oxygen-glucose Deprivation/reoxygenation (OGD/R)-induced Neuronal Injury By Inhibiting Bach1 and Promoting Nrf2/ARE Signaling. Biochem Biophys Res Commun. 2018 12 9;507(1-4):114-121. PubMed PMID: 30449595.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MicroRNA-98-5p ameliorates oxygen-glucose deprivation/reoxygenation (OGD/R)-induced neuronal injury by inhibiting Bach1 and promoting Nrf2/ARE signaling. AU - Sun,Xiuyan, AU - Li,Xiaoming, AU - Ma,Sirui, AU - Guo,Yong, AU - Li,Yanling, Y1 - 2018/11/16/ PY - 2018/10/12/received PY - 2018/10/29/accepted PY - 2018/11/20/pubmed PY - 2019/5/18/medline PY - 2018/11/20/entrez KW - Bach1 KW - Nrf2 KW - Oxygen-glucose deprivation/reoxygenation KW - miR-98-5p SP - 114 EP - 121 JF - Biochemical and biophysical research communications JO - Biochem. Biophys. Res. Commun. VL - 507 IS - 1-4 N2 - MicroRNA-98-5p (miR-98-5p) is a stress-related microRNA (miRNA) that plays an important role in regulating cell survival, apoptosis, and oxidative stress in multiple cell types and diseases. However, little is known about the role of miR-98-5p in cerebral ischemia/reperfusion injury. In this study, we investigated the role and mechanism of miR-98-5p in regulating neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R), an in vitro model of cerebral ischemia/reperfusion injury. We found that miR-98 expression was significantly altered in neurons in response to OGD/R treatment. Functional experiments showed that overexpression of miR-98-5p inhibited OGD/R-induced apoptosis and reactive oxygen species (ROS) production in neurons, whereas inhibition of miR-98-5p showed the opposite effect. Interestingly, bioinformatics analysis predicted that BTB and CNC homology 1 (Bach1) was a potential target gene of miR-98-5p, that was verified by dual-luciferase reporter assay. Moreover, overexpression of miR-98-5p inhibited Bach1 expression while suppression of miR-98-5p promoted Bach1 expression in neurons. Notably, miR-98-5p was shown to regulate the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) and the activity of the antioxidant response element (ARE). However, overexpression of Bach1 or silencing of Nrf2 significantly abolished the miR-98-5p-mediated neuroprotective effect. Overall, these results demonstrate that miR-98-5p ameliorates OGD/R-induced neuronal injury in vitro through targeting to promote activation of Nrf2/ARE signaling. Our study suggests that miR-98-5p may play a potential role in cerebral ischemia/reperfusion injury and represents a potential therapeutic target for neuroprotection. SN - 1090-2104 UR - https://www.unboundmedicine.com/medline/citation/30449595/MicroRNA_98_5p_ameliorates_oxygen_glucose_deprivation/reoxygenation__OGD/R__induced_neuronal_injury_by_inhibiting_Bach1_and_promoting_Nrf2/ARE_signaling_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-291X(18)32370-2 DB - PRIME DP - Unbound Medicine ER -