MiR-122-5p Mitigates Inflammation, Reactive Oxygen Species and SH-SY5Y Apoptosis by Targeting CPEB1 After Spinal Cord Injury Via the PI3K/AKT Signaling Pathway
Spinal cord injury (SCI) is a threatening disease that lead to severe motor and sensory deficits. Previous research has revealed that miRNAs are involved in the pathogenesis of a variety of diseases. However, whether miR-122-5p was involved in SCI was rarely investigated. In our study, we intended t...
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| Published in | Neurochemical research Vol. 46; no. 4; pp. 992 - 1005 |
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| Main Authors | , , , , , |
| Format | Journal Article |
| Language | English |
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New York
Springer US
01.04.2021
Springer Nature B.V |
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| Abstract | Spinal cord injury (SCI) is a threatening disease that lead to severe motor and sensory deficits. Previous research has revealed that miRNAs are involved in the pathogenesis of a variety of diseases. However, whether miR-122-5p was involved in SCI was rarely investigated. In our study, we intended to probe role of miR-122-5p in the regulation of inflammatory response, reactive oxygen species (ROS) and SH-SY5Y apoptosis. We found miR-122-5p was downregulated in SCI mouse model and LPS-induced SH-SY5Y cells. Moreover, miR-122-5p overexpression alleviated inflammatory response, ROS and SH-SY5Y apoptosis in SCI mice. In addition, miR-122-5p elevation also mitigated SCI in LPS-induced SH-SY5Y cells. Additionally, cytoplasmic polyadenylation element binding protein 1 (CPEB1) was verified to be a target of miR-122-5p. CPEB1 expression was upregulated in SCI mouse model and LPS-induced SH-SY5Y cells. CPEB1 expression was negatively related to miR-122-5p expression. Moreover, CPEB1 activated the PI3K/AKT signaling pathway in SH-SY5Y cells. Finally, CPEB1 elevation recovered the suppressive effect on inflammatory response, ROS and SH-SY5Y apoptosis in LPS-treated SH-SY5Y cells mediated by miR-122-5p upregulation and through the PI3K/AKT signaling pathway. |
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| AbstractList | Spinal cord injury (SCI) is a threatening disease that lead to severe motor and sensory deficits. Previous research has revealed that miRNAs are involved in the pathogenesis of a variety of diseases. However, whether miR-122-5p was involved in SCI was rarely investigated. In our study, we intended to probe role of miR-122-5p in the regulation of inflammatory response, reactive oxygen species (ROS) and SH-SY5Y apoptosis. We found miR-122-5p was downregulated in SCI mouse model and LPS-induced SH-SY5Y cells. Moreover, miR-122-5p overexpression alleviated inflammatory response, ROS and SH-SY5Y apoptosis in SCI mice. In addition, miR-122-5p elevation also mitigated SCI in LPS-induced SH-SY5Y cells. Additionally, cytoplasmic polyadenylation element binding protein 1 (CPEB1) was verified to be a target of miR-122-5p. CPEB1 expression was upregulated in SCI mouse model and LPS-induced SH-SY5Y cells. CPEB1 expression was negatively related to miR-122-5p expression. Moreover, CPEB1 activated the PI3K/AKT signaling pathway in SH-SY5Y cells. Finally, CPEB1 elevation recovered the suppressive effect on inflammatory response, ROS and SH-SY5Y apoptosis in LPS-treated SH-SY5Y cells mediated by miR-122-5p upregulation and through the PI3K/AKT signaling pathway. Spinal cord injury (SCI) is a threatening disease that lead to severe motor and sensory deficits. Previous research has revealed that miRNAs are involved in the pathogenesis of a variety of diseases. However, whether miR-122-5p was involved in SCI was rarely investigated. In our study, we intended to probe role of miR-122-5p in the regulation of inflammatory response, reactive oxygen species (ROS) and SH-SY5Y apoptosis. We found miR-122-5p was downregulated in SCI mouse model and LPS-induced SH-SY5Y cells. Moreover, miR-122-5p overexpression alleviated inflammatory response, ROS and SH-SY5Y apoptosis in SCI mice. In addition, miR-122-5p elevation also mitigated SCI in LPS-induced SH-SY5Y cells. Additionally, cytoplasmic polyadenylation element binding protein 1 (CPEB1) was verified to be a target of miR-122-5p. CPEB1 expression was upregulated in SCI mouse model and LPS-induced SH-SY5Y cells. CPEB1 expression was negatively related to miR-122-5p expression. Moreover, CPEB1 activated the PI3K/AKT signaling pathway in SH-SY5Y cells. Finally, CPEB1 elevation recovered the suppressive effect on inflammatory response, ROS and SH-SY5Y apoptosis in LPS-treated SH-SY5Y cells mediated by miR-122-5p upregulation and through the PI3K/AKT signaling pathway.Spinal cord injury (SCI) is a threatening disease that lead to severe motor and sensory deficits. Previous research has revealed that miRNAs are involved in the pathogenesis of a variety of diseases. However, whether miR-122-5p was involved in SCI was rarely investigated. In our study, we intended to probe role of miR-122-5p in the regulation of inflammatory response, reactive oxygen species (ROS) and SH-SY5Y apoptosis. We found miR-122-5p was downregulated in SCI mouse model and LPS-induced SH-SY5Y cells. Moreover, miR-122-5p overexpression alleviated inflammatory response, ROS and SH-SY5Y apoptosis in SCI mice. In addition, miR-122-5p elevation also mitigated SCI in LPS-induced SH-SY5Y cells. Additionally, cytoplasmic polyadenylation element binding protein 1 (CPEB1) was verified to be a target of miR-122-5p. CPEB1 expression was upregulated in SCI mouse model and LPS-induced SH-SY5Y cells. CPEB1 expression was negatively related to miR-122-5p expression. Moreover, CPEB1 activated the PI3K/AKT signaling pathway in SH-SY5Y cells. Finally, CPEB1 elevation recovered the suppressive effect on inflammatory response, ROS and SH-SY5Y apoptosis in LPS-treated SH-SY5Y cells mediated by miR-122-5p upregulation and through the PI3K/AKT signaling pathway. |
| Author | Wang, Binbin Wu, Ji Xie, Hao Liu, Jun Wei, Zijian Zhu, Zezhang |
| Author_xml | – sequence: 1 givenname: Zijian surname: Wei fullname: Wei, Zijian organization: Department of Orthopaedics, Sir Run Run Hospital, Nanjing Medical University, Department of Spine Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University – sequence: 2 givenname: Jun surname: Liu fullname: Liu, Jun organization: Department of Orthopaedics, Sir Run Run Hospital, Nanjing Medical University, Department of Orthopaedics, The Second Affiliated Hospital of Nanjing Medical University – sequence: 3 givenname: Hao surname: Xie fullname: Xie, Hao organization: Department of Orthopaedics, Sir Run Run Hospital, Nanjing Medical University – sequence: 4 givenname: Binbin surname: Wang fullname: Wang, Binbin organization: Department of Orthopaedics, Sir Run Run Hospital, Nanjing Medical University – sequence: 5 givenname: Ji surname: Wu fullname: Wu, Ji organization: Department of Orthopaedics, Sir Run Run Hospital, Nanjing Medical University – sequence: 6 givenname: Zezhang surname: Zhu fullname: Zhu, Zezhang email: zhuzezhang_njmu@sina.com organization: Department of Spine Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing Medical University, Department of Spine Surgery, Nanjing Drum Tower Hospital, Medical School of Nanjing University |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33528808$$D View this record in MEDLINE/PubMed |
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| Title | MiR-122-5p Mitigates Inflammation, Reactive Oxygen Species and SH-SY5Y Apoptosis by Targeting CPEB1 After Spinal Cord Injury Via the PI3K/AKT Signaling Pathway |
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