MiR-221 alleviates the inflammatory response and cell apoptosis of neuronal cell through targeting TNFAIP2 in spinal cord ischemia–reperfusion. Issue 8 (23rd May 2018)
- Record Type:
- Journal Article
- Title:
- MiR-221 alleviates the inflammatory response and cell apoptosis of neuronal cell through targeting TNFAIP2 in spinal cord ischemia–reperfusion. Issue 8 (23rd May 2018)
- Main Title:
- MiR-221 alleviates the inflammatory response and cell apoptosis of neuronal cell through targeting TNFAIP2 in spinal cord ischemia–reperfusion
- Authors:
- Zhao, Dong
Deng, Shu-Cai
Ma, Yi
Hao, Yong-Hong
Jia, Zhan-Hua - Abstract:
- 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 inflammatoryAbstract : 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. … (more)
- Is Part Of:
- NeuroReport. Volume 29:Issue 8(2018)
- Journal:
- NeuroReport
- Issue:
- Volume 29:Issue 8(2018)
- Issue Display:
- Volume 29, Issue 8 (2018)
- Year:
- 2018
- Volume:
- 29
- Issue:
- 8
- Issue Sort Value:
- 2018-0029-0008-0000
- Page Start:
- Page End:
- Publication Date:
- 2018-05-23
- Subjects:
- miR-221 -- spinal cord ischemia/reperfusion -- TNFAIP2 -- tumor necrosis factor-α
Neurosciences -- Periodicals
Nervous system -- Periodicals
Neurophysiology -- Periodicals
Nervous System Diseases -- Periodicals
Nervous System Physiological Phenomena -- Periodicals
Neurosciences -- Periodicals
616.805 - Journal URLs:
- http://journals.lww.com/neuroreport/pages/default.aspx ↗
http://www.neuroreport.com/ ↗
http://journals.lww.com/pages/default.aspx ↗
http://firstsearch.oclc.org ↗ - DOI:
- 10.1097/WNR.0000000000001013 ↗
- Languages:
- English
- ISSNs:
- 0959-4965
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- Legaldeposit
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