CLEC14A deficiency exacerbates neuronal loss by increasing blood-brain barrier permeability and inflammation.

ABSTRACT: BACKGROUND:Ischemic stroke is a main cause of mortality. Blood-brain barrier (BBB) breakdown appears to play a critical role in inflammation in patients with ischemic stroke and acceleration of brain injury. The BBB has a protective function and is composed of endothelial cells, pericytes, and astrocytes. In ischemic stroke treatments, regulation of vascular endothelial growth factor (VEGF)-A and vascular endothelial growth factor receptor (VEGFR)-2 is a crucial target despite adverse effects. Our previous study found that loss of C-type lectin family 14 member A (CLEC14A) activated VEGF-A/VEGFR-2 signaling in developmental and tumoral angiogenesis. Here, we evaluate the effects of BBB impairment caused by CLEC14A deficiency in ischemia-reperfusion injury. METHODS:In vitro fluorescein isot

SUBMITTER: Kim Y 

PROVIDER: S-EPMC7001304 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature