tailieunhanh - Báo cáo khoa học: MicroRNA-21 protects neurons from ischemic death

MicroRNAs are small RNAs that attenuate protein expression by comple-mentary binding to the 3¢-UTR of a target mRNA. Currently, very little is known about microRNAs after cerebral ischemia. In particular, micro-RNA-21 (miR-21) is a strong antiapoptotic factor in some biological systems. We investigated the role of miR-21 after stroke in the rat. | ỊFEBS Journal MicroRNA-21 protects neurons from ischemic death Ben Buller1 2 Xianshuang Liu1 Xinli Wang1 Rui L. Zhang1 Li Zhang1 Ann Hozeska-Solgot1 Michael Chopp1 2 and Zheng G. Zhang1 1 Department of Neurology Henry Ford Hospital Detroit MI USA 2 Department of Physics Oakland University Rochester MI USA Keywords microRNA miR-21 neuron neuroprotection stroke Correspondence Z. G. Zhang Henry Ford Hospital Department of Neurology 2799 West Grand Blvd Detroit MI 48202 USA Fax 1 313 916 1318 Tel 1 313 916 5456 E-mail zhazh@ Received 7 April 2010 revised 30 July 2010 accepted 18 August 2010 doi MicroRNAs are small RNAs that attenuate protein expression by complementary binding to the 3 -UTR of a target mRNA. Currently very little is known about microRNAs after cerebral ischemia. In particular micro-RNA-21 miR-21 is a strong antiapoptotic factor in some biological systems. We investigated the role of miR-21 after stroke in the rat. We employed in situ hybridization and laser capture microdissection in combination with real-time RT-PCR to investigate the expression of miR-21 after stroke. In situ hybridization revealed that miR-21 expression was upregu-lated in neurons of the ischemic boundary zone and quantitative real-time RT-PCR analysis revealed that stroke increased mature miR-21 levels by approximately threefold in neurons isolated from the ischemic boundary zone by laser capture microdissection as compared with homologous contralateral neurons 2 days n 4 P and 7 days n 3 P after stroke. In vitro overexpression of miR-21 in cultured cortical neurons substantially suppressed oxygen and glucose deprivation-induced apoptotic cell death whereas attenuation of endogenous miR-21 by antisense inhibition exacerbated cell death after oxygen and glucose deprivation. Moreover overexpression of miR-21 in neurons significantly reduced FASLG levels and introduction of an miR-21 mimic into 293-HEK cells substantially reduced

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