1.Relationship between cholecystolithiasis and long-term complications induced by endoscopic sphincte-rotomy for choledocholithiasis
Liping YE ; Yu ZHANG ; Xingli MAO ; Minhua LIN
Chinese Journal of Digestive Endoscopy 2010;27(7):350-352
Objective To explore the long-term efficacy of endoscopic sphincterotomy (EST) for choledocholithiasis and to evaluate the necessity of cholecystectomy after EST. Methods Two hundred and fifty seven patients who underwent EST for choledocholithiasis in 2006 were followed up for an average period of 34. 8 months (26-48 months). According to the existence of cholecystolithiasis, the patients were divided into group A (combined with cholecystolithiasis, n = 151) and group B (without cholecystolithiasis, n = 106) , and group A was further divided into group A1 as undergoing cholecystectomy after EST (n =56) and group A2 as not having cholecystectomy after EST ( n = 95). Results Of the 257 patients, late complications occurred in 31 patients (12. 1% ) , including recurrent choledocholithiasis in 25 (9.7% ), cholangitis in 27 (10. 1% ) , acute pancreatitis in 2 (0. 8% ) and cholangiocarcinoma in 1 (0.4% ). The rates of late complications and recurrent choledocholithiasis were significantly higher in group A2 than those in group A1 (P<0.05). Conclusion EST is safe and effective for choledocholithiasis. Cholecystectomy after EST is necessary in patients with cholecystolithiasis.
2.Overexpression of miR-155-5p Inhibits the Proliferation and Migration of IL-13-Induced Human Bronchial Smooth Muscle Cells by Suppressing TGF-β-Activated Kinase 1/MAP3K7-Binding Protein 2.
Yujia SHI ; Xingli FU ; Qi CAO ; Zhengdao MAO ; Yi CHEN ; Yun SUN ; Zhiguang LIU ; Qian ZHANG
Allergy, Asthma & Immunology Research 2018;10(3):260-267
PURPOSE: Molecular mechanisms leading to asthma is still ill-defined. Though the function of microRNAs (miRNAs) in asthma was previously reported, the involvement of miR-155 in important features of this disease remains unknown. The present study was designed to uncover the probable involvement of miR-155-5p in the proliferation and migration of IL-13-induced human bronchial smooth muscle cells (BSMCs) and the intrinsic regulatory mechanism. METHODS: The effects of different concentrations of IL-13 on the proliferation and migration of BSMCs as well as the expression of miR-155-5p and its predicted target transforming growth factor (TGF)-β-activated kinase 1/MAP3K7-binding protein 2 (TAB2) were investigated. The effects of miR-155-5p on the proliferation and migration of interleukin (IL)-13-induced BSMCs was determined in vitro using BSMCs transfected with miR-155 mimic/inhibitor and induced by a high concentration of IL-13. The quantitative real-time polymerase chain reaction (qRTPCR) was employed for determining the expression of miR-155-5p and TAB2. Western blotting was applied to analyze the expression of TAB2 at the protein level. Cell proliferation and migration were assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and Transwell assays, respectively. RESULTS: The proliferation and migration of BSMCs were dose-dependently increased with IL-13 treatment. Contrariwise, IL-13 dose-dependently inhibited the expression of miR-155-5p in BSMCs. Mechanistic studies showed that inhibition of miR-155-5p further promoted the stimulatory effects of IL-13, whereas overexpression of miR-155 significantly inhibited these effects. In silico studies and luciferase reporter assays indicated that TAB2 was a negatively regulated miR-155-5p target. CONCLUSIONS: These results suggested that miR-155-5p-inhibit the IL-13-induced proliferation and migration of BSMCs by targeting TAB2 and that the IL-13/miR-155/TAB2 pathway could serve as a therapeutic target for pulmonary diseases, especially asthma.
Asthma
;
Blotting, Western
;
Cell Proliferation
;
Computer Simulation
;
Humans*
;
In Vitro Techniques
;
Interleukin-13
;
Interleukins
;
Luciferases
;
Lung Diseases
;
MicroRNAs
;
Muscle, Smooth*
;
Myocytes, Smooth Muscle*
;
Phosphotransferases*
;
Real-Time Polymerase Chain Reaction
;
Transforming Growth Factors