ArticleJournal of molecular histology2021
miR-495 reduces neuronal cell apoptosis and relieves acute spinal cord injury through inhibiting PRDM5.
Article in Journal of molecular histology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Dynamic rewiring of microRNA networks in the brainstem autonomic control circuits during hypertension development in the female spontaneously hypertensive rat.Physiological genomics · 2025Article
- Exosomal miR-17-92 Cluster from BMSCs Alleviates Apoptosis and Inflammation in Spinal Cord Injury.Biochemical genetics · 2025Article
- Oxysophocarpine Prevents the Glutamate-Induced Apoptosis of HT-22 Cells via the Nrf2/HO-1 Signaling Pathway.Current issues in molecular biology · 2024Article
- Pathophysiology of Arginases in Cancer and Efforts in Their Pharmacological Inhibition.International journal of molecular sciences · 2024Review
- Silencing of Long Noncoding RNA Growth Arrest-Specific 5 Alleviates Neuronal Cell Apoptosis and Inflammatory Responses Through Sponging microRNA-93 to Repress PTEN Expression in Spinal Cord Injury.Frontiers in cellular neuroscience · 2021Article
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Authors and funding
4 authors.
Funding
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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.
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