{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,5]],"date-time":"2026-08-05T00:57:50Z","timestamp":1785891470267,"version":"3.56.0"},"reference-count":61,"publisher":"SAGE Publications","issue":"10","license":[{"start":{"date-parts":[[2019,10,10]],"date-time":"2019-10-10T00:00:00Z","timestamp":1570665600000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:p>\n                    Most neurological diseases, including stroke, lead to some degree of blood\u2013brain 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\u2019 role during cerebral ischemia\/reperfusion is still underexplored. Endothelial levels of miR-98 were significantly altered following ischemia\/reperfusion insults, both in\u00a0vivo and in\u00a0vitro, transient middle cerebral artery occlusion (tMCAO), and oxygen\u2013glucose deprivation (OGD), respectively. Overexpression of miR-98 reduced the mouse\u2019s infarct size after tMCAO. Further, miR-98 lessened infiltration of proinflammatory Ly6C\n                    <jats:sup>HI<\/jats:sup>\n                    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\u00a0vivo and improved transendothelial electrical resistance (TEER) in\u00a0vitro. 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.\n                  <\/jats:p>","DOI":"10.1177\/0271678x19882264","type":"journal-article","created":{"date-parts":[[2019,10,10]],"date-time":"2019-10-10T21:23:26Z","timestamp":1570742606000},"page":"1953-1965","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":104,"title":["miR-98 reduces endothelial dysfunction by protecting blood\u2013brain barrier (BBB) and improves neurological outcomes in mouse ischemia\/reperfusion stroke model"],"prefix":"10.1177","volume":"40","author":[{"given":"David L","family":"Bernstein","sequence":"first","affiliation":[{"name":"Department of Pathology and Laboratory Medicine, Temple University, Philadelphia, PA, 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