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. 2021 Apr;52(2):385-396.
doi: 10.1007/s10735-021-09959-z. Epub 2021 Feb 25.

miR-495 reduces neuronal cell apoptosis and relieves acute spinal cord injury through inhibiting PRDM5

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miR-495 reduces neuronal cell apoptosis and relieves acute spinal cord injury through inhibiting PRDM5

Yan Zhang et al. J Mol Histol. 2021 Apr.

Abstract

This study aims to investigate the role of miR-495 in neuronal cell apoptosis after acute spinal cord injury (ASCI). The ASCI rat model was established and the Basso, Beattie, and Bresnahan (BBB) score was assessed. miR-495, PR domain containing 5 (PRDM5), and Bcl-2 expressions were measured by qRT-PCR or western blotting. Neuronal cell line PC-12 was subjected to hypoxia condition to simulate the in vitro ASCI model. PC-12 cell apoptosis was measured by flow cytometry, and the interaction between miR-495 and PRDM5 was confirmed by dual luciferase reporter assay. Results showed that BBB score was significantly decreased in ASCI rats compared with sham rats. miR-495 expression was down-regulated in spinal cord tissue of ASCI rats and hypoxia-induced PC-12 cells, and PRDM5 protein level was up-regulated in spinal cord tissue of ASCI rats and hypoxia-induced PC-12 cells. miR-495 overexpression could reduce apoptosis of PC-12 cells, and up-regulated anti-apoptosis protein Bcl-2 protein level. Moreover, PRDM5 was a target of miR-495, and mRNA and protein levels of PRDM5 were negatively regulated by miR-495. miR-495 overexpression could reduce the hypoxia-induced PC-12 cell apoptosis, while PRDM5 overexpression abolished this inhibiting effect. The agomir-495 was injected into ASCI rats, and Bcl-2 protein level and BBB score were increased, but the PRDM5 overexpression reversed these results. Overall, we concluded that miR-495 could inhibit neuronal cell apoptosis and relieve acute spinal cord injury through inhibiting PRDM5.

Keywords: Acute spinal cord injury; Neuronal cell apoptosis; PC-12 cell; PRDM5; miR-495.

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References

    1. Bai Z, Wang J, Wang T, Li Y, Zhao X, Wu G, Yang Y, Deng W, Zhang Z (2017) The MiR-495/annexin A3/P53 axis inhibits the invasion and EMT of colorectal cancer cells. Cell Physiol Biochem 44(5):1882–1895 - DOI
    1. Bowes A, Yip P (2014) Modulating inflammatory cell responses to spinal cord injury: all in good time. J Neurotrauma 31(21):1753–1766 - DOI
    1. Chen G, Xie Y (2018) miR-495 inhibits proliferation, migration, and invasion and induces apoptosis via inhibiting PBX3 in melanoma cells. Onco Targets Ther 11:1909–1920 - DOI
    1. Chen Q, Xu J, Li L, Li H, Mao S, Zhang F, Zen K, Zhang C, Zhang Q (2014) MicroRNA-23a/b and microRNA-27a/b suppress Apaf-1 protein and alleviate hypoxia-induced neuronal apoptosis. Cell Death Dis 5:e1132 - DOI
    1. Chen X, Cui J, Zhai X, Zhang J, Gu Z, Zhi X, Weng W, Pan P, Cao L, Ji F et al (2018) Inhalation of hydrogen of different concentrations ameliorates spinal cord injury in mice by protecting spinal cord neurons from apoptosis, oxidative injury and mitochondrial structure damages. Cell Physiol Biochem 47(1):176–190 - DOI