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

• Published in: Neurochemical research Vol. 46; no. 4; pp. 992 - 1005
• Main Authors: Wei, Zijian, Liu, Jun, Xie, Hao, Wang, Binbin, Wu, Ji, Zhu, Zezhang
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.04.2021; Springer Nature B.V
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Animals; Apoptosis; Apoptosis - physiology; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Cell Line, Tumor; Down-Regulation - drug effects; Down-Regulation - physiology; Humans; Inflammation; Inflammation - etiology; Inflammation - metabolism; Inflammatory response; Lipopolysaccharides; Lipopolysaccharides - pharmacology; Mice; Mice, Inbred C57BL; MicroRNAs - metabolism; mRNA Cleavage and Polyadenylation Factors - metabolism; Neurochemistry; Neurology; Neurosciences; Original Paper; Pathogenesis; Phosphatidylinositol 3-Kinases - metabolism; Polyadenylation; Proto-Oncogene Proteins c-akt - metabolism; Reactive oxygen species; Reactive Oxygen Species - metabolism; Signal transduction; Signal Transduction - physiology; Signaling; Spinal cord injuries; Spinal Cord Injuries - complications; Spinal Cord Injuries - metabolism; Transcription Factors - metabolism; Up-Regulation - drug effects; Up-Regulation - physiology; CPEB1; miR-122-5p; Spinal cord injury; PI3K/AKT signaling pathway
• ISSN: 0364-3190; 1573-6903; 1573-6903
• DOI: 10.1007/s11064-021-03232-1

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.