miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene
miR-29a up-regulation in AR42J cells contributes to apoptosis via targeting TNFRSF1A gene作者机构：Department of Hepatobiliary Pancreatic Surgery People’s Hospital of Zhengzhou University School of Medicine Zhengzhou University
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2016年第22卷第20期
页 面：4881-4890页
核心收录：
学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学]
主 题：Acute edematous pancreatitis mi R-29a Apoptosis AR42J Target gene TNFRSF1A
摘 要：AIM: To investigate the expression of mi R-29 a in rat acute pancreatitis and its functional role in AR42 J cell ***: Twelve SD rats were divided into a control group and an acute edematous pancreatitis(AEP) group randomly. AEP was induced by intraperitoneal injection of L-arginine(150 mg/kg) in the AEP group and equal volume of 0.9% Na Cl was injected in the control group. The apoptosis of acinar cells in pancreatic tissue was determined by TUNEL assay. mi RNA chip assay was performed to examine the expression of mi RNAs in two groups. Besides, to further explore the role of mi R-29 a in apoptosis in vitro, recombinant rat TNF-α(50 ng/m L) was administered to treat the rat pancreatic acinar cell line AR42 J for inducing AR42 J cell apoptosis. Quantitative real-time PCR(q RT-PCR) was adopted to measure mi R-29 a expression. Then, mi RNA mimic, mi RNA antisense oligonucleotide(AMO) and control vector were used to transfect AR42 J cells. The expression of mi R-29 a was confirmed by q RT-PCR andthe apoptosis rate of AR42 J cells was detected by flow cytometry analysis. Western blot was used to detect the expression of activated caspase3. Moreover, we used bioinformatics software and luciferase assay to test whether TNFRSF1 A was the target gene of mi R-29 a. After transfection, q RT-PCR and Western blot was used to detect the expression of TNFRSF1 A in AR42 J cells after ***: The expression of mi R-29 a was much higher in the AEP group compared with the control group as displayed by the mi RNA chip assay. After inducing apoptosis of AR42 J cells in vitro, the expression of mi R-29 a was significantly increased by 1.49 ± 0.04 times in comparison with the control group. As revealed by q RT-PCR assay, the expression of mi R-29 a was 2.68 ± 0.56 times higher in the mi R-29 a mimic group relative to the control vector group, accompanied with an obviously increased acinar cell apoptosis rate(42.83 ± 1.25 vs 24.97 ± 0.15, P 0.05). Moreover, th
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