Disruption of Midkine gene reduces traumatic brain injury through the modulation of neuroinflammation.
Seiya TakadaHarutoshi SakakimaTakahiro MatsuyamaShotaro OtsukaKazuki NakanishiKosuke NorimatsuYuki ItashikiAkira TaniKiyoshi KikuchiPublished in: Journal of neuroinflammation (2020)
Our findings suggest that MK-deficiency reduced tissue infiltration of microglia/macrophages and altered their polarization status thereby reducing neuroinflammation, neuronal apoptosis, and tissue loss and improving neurological outcomes after TBI. Therefore, targeting MK to modulate neuroinflammation may represent a potential therapeutic strategy for TBI management.
Keyphrases
- traumatic brain injury
- cerebral ischemia
- severe traumatic brain injury
- oxidative stress
- inflammatory response
- endoplasmic reticulum stress
- lipopolysaccharide induced
- lps induced
- cell death
- cell cycle arrest
- copy number
- neuropathic pain
- cancer therapy
- cognitive impairment
- dna methylation
- signaling pathway
- subarachnoid hemorrhage
- spinal cord injury
- genome wide identification
- pi k akt