• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >MicroRNA-27a Suppresses Detrusor Fibrosis in Streptozotocin-Induced Diabetic Rats by Targeting PRKAA2 Through the TGF-β1/Smad3 Signaling Pathway
【24h】

MicroRNA-27a Suppresses Detrusor Fibrosis in Streptozotocin-Induced Diabetic Rats by Targeting PRKAA2 Through the TGF-β1/Smad3 Signaling Pathway

机译：MicroRNA-27a通过TGF-β1/ Smad3信号通路靶向PRKAA2抑制链脲佐菌素诱导的糖尿病大鼠逼尿肌纤维化。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Background/Aims We examined the effects of microRNA-27a (miR-27a) on detrusor fibrosis in streptozotocin (STZ)-induced diabetic rats. Methods Eighty healthy Sprague-Dawley (SD) rats were randomly allocated into control, diabetic, miR-27a mimics, mimics control, miR-27a inhibitors, inhibitors control, siRNA-PRKAA2 (siPRKAA2) and inhibitors + siPRKAA2 groups (the latter 7 groups were established as STZ-induced diabetic rat models and treated in different manners). Detrusor cell apoptosis in bladder tissues was determined through terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining. Detrusor cells were assigned to the blank, miR-27a mimics, mimics control, miR-27a inhibitors, inhibitors control, siPRKAA2 and inhibitors + siPRKAA2 groups. Flow cytometry determined the cell cycle stage and apoptosis. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blotting (WB) were used to assess the expression of miR-27a, PRKAA2, TGF-β1, Smad3, p-Smad3, fibronectin (FN), connective tissue growth (CTGF), and collagen-I (COL-I) in tissues and cells. Results Compared with the control group, the diabetic, miR-27a mimics, and siPRKAA2 groups showed reduced weight and PRKAA2 expression, but elevated blood glucose, serum creatinine (sCr), blood urea nitrogen (BUN), cell apoptosis, and expression of TGF-β1, Smad3, FN, COL-I, CTGF, and p-Smad3. The opposite trend was observed in the miR-27a inhibitors group. PRKAA2 is a target gene of miR-27a. Compared to the blank group, the miR-27a mimics and siPRKAA2 groups indicated markedly increased TGF-β1, Smad3, FN, COL-I, CTGF and p-Smad3 expression; decreased PRKAA2 expression; and increased cell apoptosis. The miR-27a inhibitors group showed the opposite trend. Conclusion These results indicate that miR-27a may contribute to detrusor fibrosis in STZ-induced diabetic rats by targeting PRKAA2 via the TGF-β1/Smad3 signaling pathway.
机译：背景/目的我们研究了microRNA-27a（miR-27a）对链脲佐菌素（STZ）诱导的糖尿病大鼠逼尿肌纤维化的影响。方法将80只健康Sprague-Dawley（SD）大鼠随机分为对照组，糖尿病，miR-27a模拟物，模拟对照，miR-27a抑制剂，抑制剂对照，siRNA-PRKAA2（siPRKAA2）和抑制剂+ siPRKAA2组（后7组）建立了STZ诱导的糖尿病大鼠模型，并以不同的方式进行了治疗。通过末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记测定（TUNEL）染色确定膀胱组织中逼尿肌细胞凋亡。将逼尿肌细胞分为空白，miR-27a模拟物，模拟物对照，miR-27a抑制剂，抑制剂对照，siPRKAA2和抑制剂+ siPRKAA2组。流式细胞仪确定了细胞周期阶段和凋亡。定量逆转录聚合酶链反应（qRT-PCR）和蛋白质印迹（WB）用于评估miR-27a，PRKAA2，TGF-β1，Smad3，p-Smad3，纤连蛋白（FN），结缔组织生长（CTGF）的表达），以及组织和细胞中的胶原蛋白I（COL-1）。结果与对照组相比，糖尿病组，miR-27a模拟组和siPRKAA2组的体重和PRKAA2表达降低，但血糖，血清肌酐（sCr），血尿素氮（BUN），细胞凋亡和TGF表达升高-β1，Smad3，FN，COL-1，CTGF和p-Smad3。在miR-27a抑制剂组中观察到相反的趋势。 PRKAA2是miR-27a的靶基因。与空白组相比，miR-27a模拟物和siPRKAA2组显示TGF-β1，Smad3，FN，COL-1，CTGF和p-Smad3表达显着增加。 PRKAA2表达降低;并增加细胞凋亡。 miR-27a抑制剂组显示相反的趋势。结论这些结果表明，miR-27a可能通过TGF-β1/ Smad3信号通路靶向PRKAA2，从而促进STZ诱导的糖尿病大鼠逼尿肌纤维化。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号