JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2014, Vol. 52 ›› Issue (7): 78-81.doi: 10.6040/j.issn.1671-7554.0.2014.087

Previous Articles     Next Articles

Expressions of TGF-β1 and α-SMA in autosomal dominant polycystic kidney disease

QUE Xinxiang, DING Sentai, WU Fei, BI Dongbin, LÜ Jiaju, DING Kejia   

  1. Department of Urology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, Shandong, China
  • Received:2014-02-23 Revised:2014-05-13 Online:2014-07-10 Published:2014-07-10

Abstract: Objective To investigate the expressions and mechanism of transforming growth factor-β1 (TGF-β1) and alpha smooth muscle actin (α-SMA) in autosomal dominant polycystic kidney disease (ADPKD). Methods According to the preoperative glomerular filtration rate (GFR) of abnormal kidney, 62 ADPKD patients were divided into two groups: high GFR group (group A, n=29), and low GFR group (group B, n=33). Another 20 patients treated with radical nephrectomy were chosen as controls(the control group). Kidney tissues from patients in groups A and B, and tumor-adjacent tissues from the controls were collected. Expressions of TGF-β1 and α-SMA of the three groups were detected with immunohistochemical method. Results TGF-β1 and α-SMA were positively expressed in groups A and B, with cord-like or patch-like distribution in the renal interstitial fibrosis area. No significant expression was found in the control group. The positive expression rate of α-SMA in groups A and B was statistically significant (P<0.05). The expressions of TGF-β1 and α-SMA were positively correlated (P<0.05). Conclusion TGF-β1 and α-SMA are highly expressed in ADPKD, both of which promote epithelial-to-mesenchymal transition, leading to renal fibrosis.

Key words: Renal fibrosis, Transforming grow factor-beta, Epithelial-to-mesenchymal transition, Autosomal dominant polycystic kidney disease, α-smooth muscle actin

CLC Number: 

  • R692
[1] Eddy A A. Molecular basis of renal fibrosis[J]. Pediatr Nephrol, 2000, 15(3-4):290-301.
[2] 臧秀娟, 刘梅, 宋莹, 等. 肾小球疾病中转化生长因子-β1与肌成纤维细胞的表达及意义[J]. 中国中西医结合肾病杂志, 2010, 11(5):386-390.
[3] Lto Y, Aten J, Bende R J, et al. Expression of connective tissue growth factor in human renal fibrosis[J]. Kidney lnt, 1998, 53(4):853-861.
[4] 郭碧林, 朱春玲. Egr-1蛋白、MMP-2、TGF-β1在肾小管间质纤维化大鼠中的表达及意义[J]. 中国现代医学杂志, 2013, 23(7):27-33.
[5] Israeli S, Amsler K, Zheleznova N, et al. Abnormalities in focal adhesion complex formation, regulation, and function in human autosomal recessive polycystic kidney disease epithelial cells[J]. Am J Physiol Cell Physiol, 2010, 298(4):C831-C846.
[6] 韩聪祥, 谢庆祥, 赵力, 等. 慢性移植肾肾病肾组织中转化生长因子β1、金属蛋白酶2、金属蛋白酶组织抑制剂1的表达及意义[J]. 中国组织工程研究与临床康复, 2009, 13(5):821-824.
[7] Kaneta S, Ishizuki S, Kasahara M, et al. Renal carbonic anhydrase activity in DBA/2FG-pcy/pcy mice with inherited polycystic kidney disease[J]. Exp Anim, 1999, 48(3):161-169.
[8] 亓敏, 梁素忍, 王娜, 等. 尿毒清对慢性肾功能衰竭大鼠肾脏纤维化的影响[J]. 山东大学学报:医学版, 2010, 48(3):57-60.
[9] 刘燕, 商黔惠, 刘婵, 等. 替米沙坦降低转化生长因子β1/Smads在高盐诱导肾脏纤维化中的表达[J]. 中华高血压杂志, 2013, 21(7):689-665.
[10] Elberg D, Jayaraman S, Turman M A, et al. Transforming growth factor-β inhibits cystogenesis in human autosomal dominant polycystic kidney epithelial cells[J]. Exp Cell Res, 2012, 318(13):1508-1516.
[11] 吕家驹, 傅强. 临床实用肾脏外科学[M]. 北京:军事医学科学出版社, 2011: 288-290.
[12] Togawa H, Nakanishi K, Mukaiyama H, et al. Epithelial-to-mesenchymal transition in cyst lining epithelial cells in an orthologous PCK rat model of autosomal-recessive polycystic kidney disease[J]. Am J Physiol Renal Physiol, 2011, 300(2):511-520.
[13] Zheng G, Lyons J G, Tan T K, et al. Disruption of E-cadherin by matrix metalloproteinase directly mediates epithelial-mesenchymal transition downstream of transforming growth factor-beta 1 in renal tubular epithelial cells[J]. Am J Pathol, 2009, 175(3):580-591.
[14] Liu Y, Dai B, Xu C, et al. Rosiglitazone inhibits transforming growth factor-β1 mediated fibrogenesis in ADPKD cyst-lining epithelial cells[J]. PLoS One, 2011, 6(12): e28915.doi:10.1371/journal.pone.0028915.Epub 2011 Dec 9.
[1] TANG Xi, HU Ya, XU Yanhua, WANG Chunlin, QIU Ping, WANG Xianghui. MiR- 498 inhibits A549 cells EMT by targeting FOXM1 [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2017, 55(4): 39-43.
[2] MA Min1, ZHANG Liang2, SHAO Guang-feng1, ZHANG Lei1, LIU Yu-qiang1. Relationship between collagen type Ⅲ in serum and
renal function in  obstructive  nephropathy
[J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2012, 50(3): 62-65.
[3] XIONG Hui1, XIA Ting2, JIANG Shaobo1, XIA Qinghua1, ZHAO Yong1, JIN Xunbo1. Effect of the renal volume on surgical occasion for patients with  autosomal dominant polycystic kidney disease [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2011, 49(8): 96-99.
[4] QI Min 1, LIANG Su-ren 1, WANG Na 1, ZHEN Jun-hui 2, FENG Jin-bo 3,HU Zhao 1. Effects of Niaoduqing on renal fibrosis of chronic renal failure rats [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2010, 48(3): 57-60.
[5] . Relationship between collagen type Ⅲ in serum and renal fibrosis in obstructive nephropathy [J]. JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES), 2009, 47(12): 29-32.
Viewed
Full text


Abstract

Cited

  Shared   
  Discussed   
No Suggested Reading articles found!