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Inhibition of microRNA-148b-3p alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and oxidative stress in HT22 hippocampal neuron via reinforcing Sestrin2/Nrf2 signalling.
Clin Exp Pharmacol Physiol. 2020 Apr; 47(4):561-570.CE

Abstract

MicroRNAs (miRNAs) have emerged as crucial regulators of neuronal injury during cerebral ischaemia/reperfusion injury. Various miRNAs are dysregulated during this pathological process; however, the precise role of these miRNAs in regulating neuronal injury remains largely unknown. In the current study, we explored the potential function of microRNA-148b-3p (miR-148b-3p) in regulating neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro, a cellular model for mimicking cerebral ischaemia/reperfusion injury. We found that miR-148b-3p expression was significantly decreased in neurons in response to OGD/R exposure. Importantly, miR-148b-3p overexpression decreased cell viability and exacerbated apoptosis and reactive oxygen species (ROS) production in OGD/R-exposed neurons. By contrast, miR-148b-3p inhibition improved cell viability and decreased apoptosis and ROS production in OGD/R-exposed neurons. Notably, Sestrin2, a cytoprotective gene, was identified as a miR-148b-3p target gene. miR-148b-3p inhibition markedly increased Sestrin2 expression as well as the activation of nuclear factor erythroid-2-related factor 2 (Nrf2) antioxidant signalling. Moreover, silencing of Sestrin2 or Nrf2 significantly reversed the miR-148-3p-inhibition-mediated protective effect in OGD/R-injured neurons. Overall, these results demonstrate that miR-148b-3p inhibition protects neurons from OGD/R-induced apoptosis and ROS production through reinforcing Nrf2 antioxidant signalling via upregulation of Sestrin2. Our study indicates that the miR-148b-3p/Sestrin2/Nrf2 axis plays an important role in regulating neuronal injury and may serve as a potential therapeutic target for providing neuroprotection during cerebral ischaemia/reperfusion injury.

Authors+Show Affiliations

Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.Department of Physiology, Shaanxi University of Chinese Medicine, Xianyang City, China.Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.Department of Otolaryngology, Southern University of Science and Technology Hospital, Shenzhen, China.Department of Anesthesiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

31868937

Citation

Du, Yin, et al. "Inhibition of microRNA-148b-3p Alleviates Oxygen-glucose Deprivation/reoxygenation-induced Apoptosis and Oxidative Stress in HT22 Hippocampal Neuron Via Reinforcing Sestrin2/Nrf2 Signalling." Clinical and Experimental Pharmacology & Physiology, vol. 47, no. 4, 2020, pp. 561-570.
Du Y, Ma X, Ma L, et al. Inhibition of microRNA-148b-3p alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and oxidative stress in HT22 hippocampal neuron via reinforcing Sestrin2/Nrf2 signalling. Clin Exp Pharmacol Physiol. 2020;47(4):561-570.
Du, Y., Ma, X., Ma, L., Li, S., Zheng, J., Lv, J., Cui, L., & Lv, J. (2020). Inhibition of microRNA-148b-3p alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and oxidative stress in HT22 hippocampal neuron via reinforcing Sestrin2/Nrf2 signalling. Clinical and Experimental Pharmacology & Physiology, 47(4), 561-570. https://doi.org/10.1111/1440-1681.13231
Du Y, et al. Inhibition of microRNA-148b-3p Alleviates Oxygen-glucose Deprivation/reoxygenation-induced Apoptosis and Oxidative Stress in HT22 Hippocampal Neuron Via Reinforcing Sestrin2/Nrf2 Signalling. Clin Exp Pharmacol Physiol. 2020;47(4):561-570. PubMed PMID: 31868937.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Inhibition of microRNA-148b-3p alleviates oxygen-glucose deprivation/reoxygenation-induced apoptosis and oxidative stress in HT22 hippocampal neuron via reinforcing Sestrin2/Nrf2 signalling. AU - Du,Yin, AU - Ma,Xiaozhen, AU - Ma,Lei, AU - Li,Siyuan, AU - Zheng,Juan, AU - Lv,Junlin, AU - Cui,Long, AU - Lv,Jianrui, Y1 - 2020/01/20/ PY - 2019/11/07/received PY - 2019/12/13/revised PY - 2019/12/14/accepted PY - 2019/12/24/pubmed PY - 2019/12/24/medline PY - 2019/12/24/entrez KW - Nrf2 KW - Sestrin2 KW - cerebral ischaemia/reperfusion injury KW - miR-148b-3p SP - 561 EP - 570 JF - Clinical and experimental pharmacology & physiology JO - Clin. Exp. Pharmacol. Physiol. VL - 47 IS - 4 N2 - MicroRNAs (miRNAs) have emerged as crucial regulators of neuronal injury during cerebral ischaemia/reperfusion injury. Various miRNAs are dysregulated during this pathological process; however, the precise role of these miRNAs in regulating neuronal injury remains largely unknown. In the current study, we explored the potential function of microRNA-148b-3p (miR-148b-3p) in regulating neuronal injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro, a cellular model for mimicking cerebral ischaemia/reperfusion injury. We found that miR-148b-3p expression was significantly decreased in neurons in response to OGD/R exposure. Importantly, miR-148b-3p overexpression decreased cell viability and exacerbated apoptosis and reactive oxygen species (ROS) production in OGD/R-exposed neurons. By contrast, miR-148b-3p inhibition improved cell viability and decreased apoptosis and ROS production in OGD/R-exposed neurons. Notably, Sestrin2, a cytoprotective gene, was identified as a miR-148b-3p target gene. miR-148b-3p inhibition markedly increased Sestrin2 expression as well as the activation of nuclear factor erythroid-2-related factor 2 (Nrf2) antioxidant signalling. Moreover, silencing of Sestrin2 or Nrf2 significantly reversed the miR-148-3p-inhibition-mediated protective effect in OGD/R-injured neurons. Overall, these results demonstrate that miR-148b-3p inhibition protects neurons from OGD/R-induced apoptosis and ROS production through reinforcing Nrf2 antioxidant signalling via upregulation of Sestrin2. Our study indicates that the miR-148b-3p/Sestrin2/Nrf2 axis plays an important role in regulating neuronal injury and may serve as a potential therapeutic target for providing neuroprotection during cerebral ischaemia/reperfusion injury. SN - 1440-1681 UR - https://www.unboundmedicine.com/medline/citation/31868937/Inhibition_of_microRNA_148b_3p_alleviates_oxygen_glucose_deprivation/reoxygenation_induced_apoptosis_and_oxidative_stress_in_HT22_hippocampal_neuron_via_reinforcing_Sestrin2/Nrf2_signalling_ L2 - https://doi.org/10.1111/1440-1681.13231 DB - PRIME DP - Unbound Medicine ER -
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