MiR‐137 inhibited inflammatory response and apoptosis after spinal cord injury via targeting of MK2

Abstract

Spinal cord injuries are common and troublesome disorder, which is mediated by various signal pathways and mechanisms. MK2 is also involved in numerous inflammatory diseases including spinal cord injury. The role of microRNA-137 (miR-137) and its detailed working mechanism in spinal cord injuries remain unclear. In the present study, we found that an elevated MK2 but a decreased miR-137 was expressed in serum specimens of patients with spinal cord injury and in hydrogen peroxide-treated C8-D1A and C8-B4 cells. Meanwhile, we suggested that upregulation of miR-137 could inhibit the expression of TNF-α and IL-6, two markers of inflammatory response after SCI, and apoptosis in hydrogen peroxide-treated C8-D1A and C8-B4 cells. Furthermore, we verified that MK2 was a direct target of miR-137 thorough a constructed luciferase assay. Even further, we elucidated that miR-137 could suppress the inflammatory response and apoptosis via negative regulation of MK2. Finally, through an animal model trial performed using mice, we demonstrated the protective effect of how miR-137 works on inflammatory response and apoptosis after spinal cord injury. Considering all the forementioned, our findings revealed that miR-137 inhibited inflammatory response and apoptosis after spinal cord injury via the targeting of MK2. The outcomes of the present study might indicate a new target in molecular treatment of SCI.

MicroRNA-92a-3p enhances functional recovery and suppresses apoptosis after spinal cord injury via targeting phosphatase and tensin homolog

“…SCI is a serious CNS injury and can result in permanent movement disorders, cognition impairment and even paralysis [26]. Although it has been widely discovered that the mechanisms underlying the secondary injury of SCI involve numerous molecular and biochemical changes such as inflammatory activation, production of free radicals, axonal plasticity and neuronal cell death [27], SCI still remains one of the major challenges in clinical practice [28].…”

MicroRNA-362-3p attenuates motor deficit following spinal cord injury via targeting paired box gene 2

“…For example, miR-544a level was significantly reduced after SCI and its high expression level alleviated the inflammation and took part in the recovery of SCI (Yang et al, 2018). Moreover, previous studies revealed that miR-137 could show the suppressive effect on the inflammatory response and apoptosis after SCI (Gao et al, 2018). Importantly, it is interesting that miR-362-3p could be regulated after SCI, which demonstrated by previous research (Zhu et al, 2017).…”

Curcumin alleviates LPS-induced inflammation and oxidative stress in mouse microglial BV2 cells by targeting miR-137-3p/NeuroD1

“…Considering the vital functions of miR-137-3p 19,20,22,26 and Neu-roD1 (ref. 14, 27 and 28) in the nervous system, we investigated their role in the SCI cell model.…”

“…15,16 The imbalance of miRNA is related to a variety of central nervous system diseases, and additionally, it is also associated with glial differentiation. 17,18 miRNA (miR)-137-3p, a welldocumented tumor repressor, has been reported to function in SCI mice/rat models 19,20 induced by spinal cord contusion, as well as in SCI cell models induced by high glucose and H 2 O 2 . 21,22 Besides, the down-regulation of miR-137-3p is invariably observed in the serum from SCI patients, rat SCI models, and H 2 O 2 -induced astrocytes in vitro.…”

“…21,22 Besides, the down-regulation of miR-137-3p is invariably observed in the serum from SCI patients, rat SCI models, and H 2 O 2 -induced astrocytes in vitro. 19,20 However, the role of miR-137-3p and its detailed working mechanism in SCI has not been fully elucidated to date. Although evidence has suggested miRNAs as one of the important targets for curcumin when exhibiting its anti-cancer properties, 23,24 little is known about the contribution of miRNAs on the role of curcumin in SCI.…”