Cathepsin H deficiency decreases hypoxia-ischemia-induced hippocampal atrophy in neonatal mice through attenuated TLR3/IFN-β signaling.
Junjun NiJuan ZhaoXinwen ZhangThomas ReinheckelVito TurkHiroshi NakanishiPublished in: Journal of neuroinflammation (2021)
These observations suggest that CatH plays a critical role in the proteolytic maturation and stabilization of TLR3, which is necessary for IFN-β production. Therefore, impaired TLR3/IFN-β signaling resulting from CatH deficiency may induce microglial cell death after activation and astrogliosis/glial scar formation in the hippocampus following HI injury, leading to suppression of hippocampal atrophy.
Keyphrases
- immune response
- inflammatory response
- toll like receptor
- cell death
- dendritic cells
- cerebral ischemia
- lipopolysaccharide induced
- nuclear factor
- lps induced
- neuropathic pain
- replacement therapy
- high glucose
- high fat diet induced
- diabetic rats
- blood brain barrier
- adipose tissue
- insulin resistance
- cognitive impairment
- spinal cord
- oxidative stress
- cell proliferation
- skeletal muscle
- wild type
- smoking cessation