Hypoxia-induced miR-210 modulates gene expression in response to acute peripheral ischemia.. Mus musculus

Peripheral Artery Disease is caused by the restriction or occlusion of arteries supplying the leg. Better understanding of the molecular mechanisms underpinning tissue response to acute and chronic ischemia is urgently needed to improve therapeutic options. The aim of this study is understanding miR-210 regulation and role in a mouse model of hindlimb ischemia. Overall design: To investigate miR-210 function, mice were injected with a miR-210 complementary LNA-oligonucleotide (anti-miR-210). Then, the left femoral artery was dissected in order to induce unilateral hindlimb ischemia. Mice were sacrified 3 days later and gene expression profiles of gastrocnemius muscles were obatained.

外周动脉疾病（Peripheral Artery Disease）由供应下肢的动脉狭窄或闭塞引发。当前亟需阐明介导组织对急性与慢性缺血产生应答的分子机制，以优化临床治疗策略。本研究旨在明确miR-210在下肢缺血小鼠模型中的调控模式与生物学功能。实验设计：为探究miR-210的功能，研究者向小鼠注射miR-210互补锁核酸寡核苷酸（LNA-oligonucleotide，anti-miR-210）。随后分离左侧股动脉以构建单侧下肢缺血模型。造模3天后处死小鼠，获取其腓肠肌的基因表达谱。