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1.
Chinese Journal of Tissue Engineering Research ; (53): 6752-6757, 2014.
Article in Chinese | WPRIM | ID: wpr-475353

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. OBJECTIVE:To investigate the possible interactions between microRNA-17 and arginase II in hypoxic human pulmonary artery smooth muscle cells. 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.

2.
Chinese Journal of General Surgery ; (12)2001.
Article in Chinese | WPRIM | ID: wpr-519686

ABSTRACT

Objective To study the effect of various treatments for the Budd-Chiari syndrome (BCS). Methods The clinical data of different treatments in 260 BCS patients were analysed retrospectively. Results Of the 260 patients,273times of BCS underwent interventional treatment?operative treatment or the combination of operation and interventional therapy, including percutaneous transluminal angioplasty(PTA) or/and stenting of the inferior vena cava(IVC)in 149 cases (160 times), percutaneous transhepatic angioplasty or/and stenting of the hepatic venous in 15 cases (17 times ),the combination of the two methods in 10 cases,radical resection in room temperature in 8 cases, mesocaval shunt in 16 cases,mesojugular shunt in 5 cases,mesoatriumr shunt in 8 cases,IVC-atrium shunt in 6 cases,splenopneumoexy in 18 cases, mesocaval shunt combined with PTA and stenting of the IVC in 17 cases, and transcardic membranotomy combined with PTA and stenting of the IVC in 8 cases . Two patients died in the operation:One died of cardiac tamponade,and the another died of operrative hemorrhagic shock.During the follow-up period of 3 months~6 years,20 patients recurred,of whom 7 died of hepatic failure,the other patients recovered satisfacorily. Conclusions The interventional treatment is the first choice for BCS.For patients unable to get interventional treatments or failure for interventional treatments, operation or operation combined with interventional therapy should be considered.

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