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LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
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LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
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LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1

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LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1
Journal Article

LncRNA SNHG14 promotes inflammatory response induced by cerebral ischemia/reperfusion injury through regulating miR-136-5p /ROCK1

2019
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Overview
Recently, long non-coding RNAs (lncRNAs) are considered as critical regulators in pathogenesis progression of cerebral ischemia. In present study, lncRNA-small nucleolar RNA host gene 14 (SNHG14) was found upregulated in middle cerebral artery occlusion/reperfusion (MCAO/R) treated brain tissues and oxygen-glucose deprivation and reoxygenation (OGD/R) treated PC-12 cells. Interference of SNHG14 by shRNA vector enhanced neuron survival and suppressed inflammation in response to OGD/R insult. SNHG14 positively regulated the expression of Rho-associated coiled-coil-containing protein kinase 1 (ROCK1) via acting as a sponge of microRNA (miR)-136–5p. SNHG14 promoted neurological impairment and inflammatory response through elevating the expression of ROCK1 while decreasing miR-136–5p level in OGD/R induced damage. Collectively, we illustrated that SNHG14 could be a novel strategy for treatment ischemia stoke.