Abstract
Background: Radiation therapy is widely used for the treatment of pituitary adenomas. Unfortunately, it might raise the risk of ischemic stroke, with neuroinflammation being a major pathological process. Astrocytes are the most abundant cell type in the central nervous system and have been reported for playing important roles in ischemic stroke.
Objective: Here we studied how γ-radiation would introduce astrocytes into a detrimental state for neuroinflammation and provide new theory evidence and target for the clinical management of inflammation- related neural damage after radiation-induced ischemic stroke.
Method: HA-1800 cells were treated with γ-radiation and then the protein and mRNA levels of Connexin (Cx)-43 were evaluated by western and q-PCR. The culture supernatant was collected and the concentrations of the inflammatory factors were determined by ELISA. MiRNA complementary to Cx-43 was designed through the online tools.
Results: Cx-43 is upregulated in the treatment of γ-radiation in astrocytes and γ-radiation introduced the detrimental function of astrocytes: cell viability was reduced while the apoptotic cells were increased. Inflammatory factors like tumor necrosis factor alpha, interferon gamma, interleukin-6, interleukin 1-beta were dramatically up-regulated by the irradiation. MiR-374a rescued irradiation induced Cx-43 up-regulation of astrocytes and eliminated detrimental function triggered by γ-radiation.
Conclusion: Cx-43 expression level may play an important role in the inflammation-related neural damage after irradiation-induced ischemic stroke.
Keywords: Ischemia, Stroke, Cx-43, Astrocytes, MiR-374a, neuroinflammation.
CNS & Neurological Disorders - Drug Targets
Title:Upregulation of Connexin-43 is Critical for Irradiation-induced Neuroinflammation
Volume: 17 Issue: 7
Author(s): Wei Chen, Wusong Tong, Yijun Guo, Bin He, Lei Chen, Wenjin Yang, Chenxing Wu, Dabin Ren, Ping Zheng*Jiugeng Feng*
Affiliation:
- Shanghai University of Medicine & Health Sciences, 279 ZhouZhu Road, Pudong New Area, 200120, Shanghai,China
- Department of Neurosurgery, The First Affiliated Hospital of Nanchang University, Yong Wai Zheng Street 17, Nanchang 330006,China
Keywords: Ischemia, Stroke, Cx-43, Astrocytes, MiR-374a, neuroinflammation.
Abstract: Background: Radiation therapy is widely used for the treatment of pituitary adenomas. Unfortunately, it might raise the risk of ischemic stroke, with neuroinflammation being a major pathological process. Astrocytes are the most abundant cell type in the central nervous system and have been reported for playing important roles in ischemic stroke.
Objective: Here we studied how γ-radiation would introduce astrocytes into a detrimental state for neuroinflammation and provide new theory evidence and target for the clinical management of inflammation- related neural damage after radiation-induced ischemic stroke.
Method: HA-1800 cells were treated with γ-radiation and then the protein and mRNA levels of Connexin (Cx)-43 were evaluated by western and q-PCR. The culture supernatant was collected and the concentrations of the inflammatory factors were determined by ELISA. MiRNA complementary to Cx-43 was designed through the online tools.
Results: Cx-43 is upregulated in the treatment of γ-radiation in astrocytes and γ-radiation introduced the detrimental function of astrocytes: cell viability was reduced while the apoptotic cells were increased. Inflammatory factors like tumor necrosis factor alpha, interferon gamma, interleukin-6, interleukin 1-beta were dramatically up-regulated by the irradiation. MiR-374a rescued irradiation induced Cx-43 up-regulation of astrocytes and eliminated detrimental function triggered by γ-radiation.
Conclusion: Cx-43 expression level may play an important role in the inflammation-related neural damage after irradiation-induced ischemic stroke.
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Cite this article as:
Chen Wei , Tong Wusong, Guo Yijun , He Bin, Chen Lei , Yang Wenjin, Wu Chenxing , Ren Dabin, Zheng Ping *, Feng Jiugeng *, Upregulation of Connexin-43 is Critical for Irradiation-induced Neuroinflammation, CNS & Neurological Disorders - Drug Targets 2018; 17 (7) . https://dx.doi.org/10.2174/1871527317666180706124602
DOI https://dx.doi.org/10.2174/1871527317666180706124602 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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