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Updated: Feb 8, 2026

Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption
Published on: October 4, 2019
Upregulation of Connexin-43 is Critical for Irradiation-induced Neuroinflammation
Wei Chen1, Wusong Tong1, Yijun Guo1
1The People's Hospital of Pudong New Area, 490 South Chuanhuan Road, Chuansha New Town, Shanghai 201299, China.
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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