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Elevated Cerebral Cortical CD24 Levels in Patients and Mice with Traumatic Brain Injury: A Potential Negative Role in Nuclear Factor Kappa B/Inflammatory Factor Pathway
Authors:Wei Li  Hai-Ping Ling  Wan-Chun You  Huan-Dong Liu  Qing Sun  Meng-Liang Zhou  Wei Shen  Jin-Bing Zhao  Lin Zhu  Chun-Hua Hang
Institution:1. Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, Jiangsu Province, People’s Republic of China
2. Department of Neurosurgery, Jinling Hospital, School of Medicine, Southern Medical University (Guangzhou), 305 East Zhongshan Road, Nanjing, 210002, Jiangsu Province, People’s Republic of China
3. Department of Neurosurgery, Nanjing Brain Hospital, Affiliated to Nanjing Medical University, 264 Guangzhou Road, Nanjing, 210029, Jiangsu Province, People’s Republic of China
Abstract:Increasing evidence indicates that sterile inflammatory response contributes to secondary brain injury following traumatic brain injury (TBI). However, the specific mechanisms remain largely unknown, as is whether CD24, known as an important regulator in the non-infectious inflammatory response, plays a role in secondary brain injury after TBI. Here, the expression of CD24 was detected in samples from patients with TBI by quantitative real-time polymerase chain reaction (PCR), western blotting, immunohistochemistry and immunofluorescence. RNA interference was used to investigate the effects of CD24 on inflammatory response in a mouse model of TBI. Nuclear factor kappa B (NF-κB) DNA-binding activity was measured by electrophoretic mobility shift assay, and the levels of downstream pro-inflammatory cytokines tumor necrosis factor-α (TNF-α) and Interleukin 1β (IL-1β) were detected by real-time PCR. The results indicated that both the mRNA and protein levels of CD24 were markedly elevated after TBI in humans and mice, showing a time-dependent expression. The expression of CD24 could be observed in neurons, astrocytes and microglia in both humans and mice. Meanwhile, downregulation of CD24 significantly induced an increase of NF-κB DNA-binding activity and mRNA levels of TNF-α and IL-1β. These findings indicated that CD24 expression could negatively regulate the NF-κB/inflammatory factor pathway after experimental TBI in mice, thus providing a novel target for therapeutic intervention of TBI.
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