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miR-98 reduces endothelial dysfunction by protecting blood-brain barrier (BBB) and improves neurological outcomes in mouse ischemia/reperfusion stroke model
Journal article   Open access   Peer reviewed

miR-98 reduces endothelial dysfunction by protecting blood-brain barrier (BBB) and improves neurological outcomes in mouse ischemia/reperfusion stroke model

David L. Bernstein, Viviana Zuluaga-Ramirez, Sachin Gajghate, Nancy L. Reichenbach, Boris Polyak, Yuri Persidsky and Slava Rom
Journal of cerebral blood flow and metabolism, v 40(10), pp 1953-1965
01 Oct 2020
PMID: 31601141
url
https://doi.org/10.1177/0271678x19882264View
Published, Version of Record (VoR) Open
url
https://doi.org/10.1177/0271678X19882264View
Published, Version of Record (VoR) Open

Abstract

Endocrinology & Metabolism Hematology Life Sciences & Biomedicine Neurosciences Neurosciences & Neurology Science & Technology
Most neurological diseases, including stroke, lead to some degree of blood-brain barrier (BBB) dysfunction. A significant portion of BBB injury is caused by inflammation, due to pro-inflammatory factors produced in the brain, and by leukocyte engagement of the brain endothelium. Recently, microRNAs (miRNAs) have appeared as major regulators of inflammation-induced changes to gene expression in the microvascular endothelial cells (BMVEC) that comprise the BBB. However, miRNAs' role during cerebral ischemia/reperfusion is still underexplored. Endothelial levels of miR-98 were significantly altered following ischemia/reperfusion insults, both in vivo and in vitro, transient middle cerebral artery occlusion (tMCAO), and oxygen-glucose deprivation (OGD), respectively. Overexpression of miR-98 reduced the mouse's infarct size after tMCAO. Further, miR-98 lessened infiltration of proinflammatory Ly6C(HI) leukocytes into the brain following stroke and diminished the prevalence of M1 (activated) microglia within the impacted area. miR-98 attenuated BBB permeability, as demonstrated by changes to fluorescently-labeled dextran penetration in vivo and improved transendothelial electrical resistance (TEER) in vitro. Treatment with miR-98 improved significantly the locomotor impairment. Our study provides identification and functional assessment of miRNAs in brain endothelium and lays the groundwork for improving therapeutic approaches for patients suffering from ischemic attacks.

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Collaboration types
Domestic collaboration
Web of Science research areas
Endocrinology & Metabolism
Hematology
Neurosciences
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