期刊
FASEB JOURNAL
卷 32, 期 2, 页码 935-944出版社
FEDERATION AMER SOC EXP BIOL
DOI: 10.1096/fj.201700139RRR
关键词
ischemic stroke; rats; BMECs; occludin
资金
- National Natural Science Foundation of China [81301001, 81571119, 81371311, 81571139, 81671147, 81301002, 81400969, 81400970, 81601027]
- National Key Research and Development Program of China [2016YFC1300600]
- National Research Foundation for the Doctoral Program of Higher Education of China [20120142110068]
- New Century Excellent Talents in University [NCET-10-0406]
Blood-brain barrier (BBB) disruption plays a critical role in brain injury induced by cerebral ischemia, and preserving BBB integrity during ischemia could alleviate cerebral injury. We examined the role of miR-130a in ischemic BBB disruption by using models of rat middle cerebral artery occlusion and cell oxygen-glucose deprivation. We found that ischemia significantly increased microRNA-130a (miR-130a) level and that miR-130a was predominantly from brain microvascular endothelial cells. Antagomir-130a, an antagonist of miR-130a, could attenuate brain edema, lower BBB permeability, reduce infarct volume, and improve neurologic function. MiR-130a overexpression induced by miR-130a mimic increased monolayer permeability, and intercellular inhibition of miR-130a by a miR-130a inhibitor suppressed oxygen-glucose deprivation-induced increase in monolayer permeability. Moreover, dual luciferase reporter system showed that Homeobox A5 was the direct target of miR-130a. MiR-130a, by inhibiting Homeobox A5 expression, could down-regulate occludin, thereby increasing BBB permeability. Our results suggested that miR-130a might be implicated in ischemia-induced BBB dysfunction and serve as a target for the treatment of ischemic stroke.
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