Extracellular cold-inducible RNA-binding protein mediated neuroinflammation and neuronal apoptosis after traumatic brain injury.
Yu-Xiao LiuMing ZhaoYang YuJing-Peng LiuWen-Jia LiuRen-Qi YaoJing WangRong-Li YangYao WuNing DongYang CaoShou-Chun LiQing-Hong ZhangRun-Min YanYong-Ming YaoPublished in: Burns & trauma (2024)
These results suggest that TBI obviously enhances the secretion of eCIRP, thereby resulting in neural damage and inflammation in TBI. eCIRP may be a biomarker of TBI that can mediate the apoptosis of neuronal cells through the ERS apoptotic pathway and regulate the inflammatory response of microglia via histone modification.
Keyphrases
- cell cycle arrest
- traumatic brain injury
- cell death
- inflammatory response
- oxidative stress
- induced apoptosis
- endoplasmic reticulum stress
- lipopolysaccharide induced
- severe traumatic brain injury
- binding protein
- lps induced
- pi k akt
- mild traumatic brain injury
- cerebral ischemia
- toll like receptor
- dna methylation
- signaling pathway
- anti inflammatory
- cell proliferation
- cognitive impairment
- immune response
- gene expression
- nucleic acid