ScholarWorks@숙명여자대학교

초록

In this study, we show that ANKS1A is specifically expressed in the brain endothelial cells of adult mice. ANKS1A deficiency in adult mice does notaffect the differentiation, growth, or patterning of the cerebrovascular system; however, its absence significantly impacts the cerebrovascular systemof the aged brain. In aged ANKS1A knock-out (KO) brains, vessel lesions exhibiting cerebral cavernous malformations (CCMs) are observed. In addition, CCM-like lesions show localized peripheral blood leakage into the brain. The CCM-like lesions reveal immune cells infiltrating theparenchyma. The CCM-like lesions also contain significantly fewer astrocyte endfeets and tight junctions, indicating that the integrity of the BBBhas been partially compromised. CCM-like lesions display increased fibronectin expression in blood vessels, which is also confirmed in culturedendothelial cells deficient for ANKS1A . Therefore, we hypothesize that ANKS1A may play a role in maintaining or stabilizing healthy blood vesselsin the brain during aging.

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