miR-221 alleviates the inflammatory response and cell apoptosis of neuronal cell through targeting TNFAIP2 in spinal cord ischemia–reperfusion

    loading  Checking for direct PDF access through Ovid

Abstract

This study aimed to examine the role of miR-221 in inflammatory response and apoptosis of neuronal cells after spinal cord ischemia/reperfusion (I/R) injury. Blood samples were obtained from 20 I/R patients and that of 20 healthy individuals were used as a control. AGE1.HN and SY-SH-5Y neuronal cell lines subjected to oxygen–glucose deprivation (OGD) stress were used in cell experiments. Real-time PCR and western blot were used to evaluate the expression of miR-221, tumor necrosis factor-α, and TNFAIP2. TUNEL assay analyzed cell apoptosis. I/R patients had lower serum levels of miR-221 than healthy controls. In OGD-AGE1.HN and SY-SH-5Y cells, miR-221 was significantly downregulated and TNFAIP2 mRNA and protein were upregulated; meanwhile, both proinflammatory cytokine tumor necrosis factor-α and anti-inflammation cytokine interleukin-6 were elevated and the percentage of apoptotic cells was increased. This inflammatory response and cell apoptosis induced by OGD stress were attenuated by miR-221 overexpression and enhanced by miR-221 knockdown. TNFAIP2 is a target gene for miR-221 and could be regulated negatively by the miR-221 mimic or the miR-221 inhibitor with or without OGD stress. Accordingly, TNFAIP2 overexpression reversed the inflammatory response and cell apoptosis induced by miR-221 under OGD stress. Downregulation of miR-221 occurs in spinal cord I/R injury and in cell lines subjected to oxygen–glucose deprivation. miR-221 regulates the inflammatory response and apoptosis of neuronal cells through its impact on TNFAIP2.

Related Topics

    loading  Loading Related Articles