Brain-derived endothelial cells are neuroprotective in a chronic cerebral hypoperfusion mouse model.
Yuichi MatsuiFumitaka MuramatsuHajime NakamuraYoshimi NodaKinnosuke MatsumotoHaruhiko KishimaNobuyuki TakakuraPublished in: Communications biology (2024)
Whether organ-specific regeneration is induced by organ-specific endothelial cells (ECs) remains unelucidated. The formation of white matter lesions due to chronic cerebral hypoperfusion causes cognitive decline, depression, motor dysfunction, and even acute ischemic stroke. Vascular ECs are an important target for treating chronic cerebral hypoperfusion. Brain-derived ECs transplanted into a mouse chronic cerebral hypoperfusion model showed excellent angiogenic potential. They were also associated with reducing both white matter lesions and brain dysfunction possibly due to the high expression of neuroprotective humoral factors. The in vitro coculture of brain cells with ECs from several diverse organs suggested the function of brain-derived endothelium is affected within a brain environment due to netrin-1 and Unc 5B systems. We found brain CD157-positive ECs were more proliferative and beneficial in a mouse model of chronic cerebral hypoperfusion than CD157-negative ECs upon inoculation. We propose novel methods to improve the symptoms of chronic cerebral hypoperfusion using CD157-positive ECs.
Keyphrases
- white matter
- cerebral ischemia
- subarachnoid hemorrhage
- resting state
- cognitive impairment
- endothelial cells
- cognitive decline
- mouse model
- multiple sclerosis
- brain injury
- acute ischemic stroke
- functional connectivity
- blood brain barrier
- stem cells
- mild cognitive impairment
- poor prognosis
- risk assessment
- nitric oxide
- cell death
- sleep quality
- climate change
- nk cells
- long non coding rna
- binding protein
- high glucose