title: Elevated cerebral cortical CD24 levels in patients and mice with traumatic brain injury: a potential negative role in nuclear factor κb/inflammatory factor pathway.
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.
authors.affiliation: Department of Neurosurgery, Jinling Hospital, School of Medicine, Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, Jiangsu Province, People's Republic of China.
authors.forename: Wei
authors.initials: W
authors.lastname: Li
authors.forename: Hai-Ping
authors.initials: HP
authors.lastname: Ling
authors.forename: Wan-Chun
authors.initials: WC
authors.lastname: You
authors.forename: Huan-Dong
authors.initials: HD
authors.lastname: Liu
authors.forename: Qing
authors.initials: Q
authors.lastname: Sun
authors.forename: Meng-Liang
authors.initials: ML
authors.lastname: Zhou
authors.forename: Wei
authors.initials: W
authors.lastname: Shen
authors.forename: Jin-Bing
authors.initials: JB
authors.lastname: Zhao
authors.forename: Lin
authors.initials: L
authors.lastname: Zhu
authors.forename: Chun-Hua
authors.initials: CH
authors.lastname: Hang
mesh_terms: D000328:Adult; D000818:Animals; D001253:Astrocytes / Q000378:metabolism / Q000473:pathology; D001930:Brain Injuries / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D051927:CD24 Antigen / Q000096:biosynthesis* / Q000235:genetics; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D004268:DNA-Binding Proteins / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D015536:Down-Regulation / Q000235:genetics*; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000502:physiology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D017628:Microglia / Q000378:metabolism / Q000473:pathology; D008875:Middle Aged; D016328:NF-kappa B / Q000096:biosynthesis* / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis; D015398:Signal Transduction / Q000235:genetics*; D055815:Young Adult
chemical_list: D051927:CD24 Antigen; C497889:CD24 protein, human; D004268:DNA-Binding Proteins; D018836:Inflammation Mediators; D016328:NF-kappa B; D012333:RNA, Messenger