The interaction between arginase II and microRNA-17 in human pulmonary artery smooth muscle cells

Jin You-peng; Pang Ting-ting; Wang Wei; Wang Yu-lin

doi:10.3969/j.issn.2095-4344.2014.42.006

Abstract：BACKGROUND:microRNA-17 is confirmed to play an important role in the development of pulmonary hypertension. Some research has shown that hypoxia-induced proliferation in human pulmonary artery smooth muscle celldepends on the induction of arginase II. There is no report about whether there is some interaction between microRNA-17 and arginase II in human pulmonary artery smooth muscle cells. <br> OBJECTIVE:To investigate the possible interactions between microRNA-17 and arginase II in hypoxic human pulmonary artery smooth muscle cells. <br> METHODS:Passage 4 human pulmonary artery smooth muscle cells were cultured in 21%O 2 and 5%CO 2 (normoxia) or 1%O 2 and 5%CO 2 (hypoxia), and then transfected with mimic or inhibitor of microRNA-17 or arginase II-smal interfering RNA. RNA, microRNA and protein were isolated separately. Expression of microRNA-17 and arginase II was detected with real-time quantitative PCR and western blot assay. RESULTS AND CONCLUSION:The level of microRNA-17 was significantly increased in cultured human pulmonary artery smooth muscle cells exposed to 1%O 2 hypoxia, as was arginase II mRNA and protein expression. Furthermore, inhibition of microRNA-17 expression decreased the mRNA and protein levels of arginase II in the human pulmonary artery smooth muscle cells under hypoxia. Conversely, over-expression of microRNA-17 increased the mRNA and protein levels of arginase II in the human pulmonary artery smooth muscle cells under normoxia and hypoxia. Knockdown of arginase II by siRNA abolished the hypoxia-induced up-regulation of microRNA-17 expression. These findings indicate that arginase II is a target gene of microRNA-17 and can regulate the expression of microRNA-17 in human pulmonary artery smooth muscle cells.