期刊文献+

难治性肾病综合征患者尿miRNA-192、miRNA-29c表达及意义 被引量:4

下载PDF
导出
摘要 目的探讨尿miRNA-192、miRNA-29c在难治性肾病综合征(RNS)患者尿液中的表达及意义。方法选择RNS患者44例,包括局灶节段硬化肾小球肾炎(FSGS)20例(FSGS组)、膜性肾病(MN)6例(MN组)、系膜增生性肾小球肾炎(MsPGN)18例(MsPGN组),健康对照组15例为健康志愿者。采用RT-PCR法检测四组尿液miRNA-192、miRNA-29c的表达。结果 MsPGN组miR-192表达水平高于健康对照组(P<0.05)。FSGS组miR-29c表达水平低于健康对照组(P<0.05)。结论 RNS患者尿miR-192表达增高、miR-29c表达降低,尿miRNA-192、miRNA-29c检测有助于判断肾小球细胞外基质蓄和及肾间质纤维化的程度,可作为辅助判定RNS病理类型的检测指标。
出处 《山东医药》 CAS 2014年第22期38-39,共2页 Shandong Medical Journal
基金 广东省科技技术厅-广东省中医药科学院联合科研专项项目(2011B03220001)
  • 相关文献

参考文献8

  • 1Ogawa T, Iizuka M, Sekiya Y, et al. Suppression of type I collagen production by microRNA-29b in cultured human stellate cells[ J]. Biochem Biophys Res Commun, 2010,391 (1) :316-321.
  • 2冯英,胡昭,张佼佼.糖尿病肾病大鼠肾组织中TSP-1、TGF-β、APP、VEGF、ColⅠ的表达及意义[J].山东医药,2013,53(28):5-8. 被引量:5
  • 3Sun Y, Koo S, White N, et al. Development of a micro-array to detect human and mouse microRNAs and characterization of expres- sion in human organs [ J ]. Nucleic Acids Res, 2004,32 ( 22 ) : 188.
  • 4Kato M, Zhang L, Wang M, et al. MicroRNA-192 in diabetic kid- ney glomeruli and its function in TGF-beta-induced collagen ex- pression via inhibition of E-box repressors[ J]. Proc Natl Acad Sci USA, 2007,104(9) :3432-3437.
  • 5Patrick DM, Montgomery RL, Qi X, et al. Stress-dependent cardi- ac remodeling occurs in the absence of microRNA-21 in mice[ J]. J Clin Invest, 2010,120( 11 ) :3912-3916.
  • 6Gregory PA, Bracken CP, Smith E, et al. An autocrine TGFbeta/ ZEB/miR-200 signaling network regulates establishment and main- tenance of epithelial-mesenchymal transition [ J ]. Mol Biol Cell, 2011,22 (10) : 1686-1698.
  • 7Wang B, Herman-Edelstein M, Koh P, et al. E-cadherin expres- sion is regulated by miR-192/215 by a mechanism that is inde- pendent of the profibrotic effects of transforming growth factor-beta [ J]. Diabetes, 2010,59 (7) : 1794-1802.
  • 8Bazzi C, Petrini C, Rizza V, et al. Urinary N acetyl beta glu- cosaminidase excretion is a marker of tubular cell dysfunction and a predictor of outcome in primary glomerulonephritis [ J ]. Nephrol Dial Transplant, 2002,17(11) :890-896.

二级参考文献18

  • 1Meek RL, Cooney SK, Flynn SD, et al. Amino acids induce indica- tors of response to injury in glomerular mesangial cells [ J ]. Am J Physiol Renal Physiol, 2003,285 ( 1 ) :F79-86.
  • 2Hugo C. The thrombospondin 1-TGF-β axis in fibrotic renal disease [ J ]. Nephrol Dial Transplant, 2003,18 (7) : 1241-1245.
  • 3Hohenstein B, Daniel C, Hausknecht B, et al. Correlation of en- hanced thrombospondin-1 expression, TGF-βsignalling and protein- uria in human type-2 diabetic nephropathy[ J]. Nephrol Dial Trans- plant, 2008,23(12) :3880-3887.
  • 4Daniel C, Schaub K, Amann K, et al. Thmmbospondin-1 is an en- dogenous activator of TGF-beta in experimental diabetic nephropathy in vivo[J]. Diabetes, 2007,56(12) :2982-2989.
  • 5Karakus SC, Turkyilmaz Z, Sonmez K, et al. The effect of enala- pril on renal resistive index, urine electrolyte levels and TGF-β1 levels of kidney tissues in rats with unilateral partial ureteropelvic junction obstruction [ J]. Eur J Pediatr Surg, 2011, 1 ( 6 ) : 356-361.
  • 6Gross JL, de Azevedo M J, Silveiro SP, et al. Diabetic nephropa- thy: diagnosis, prevention and treatment [ J ]. Diabetes Care, 2005,28 ( 1 ) : 164-176.
  • 7Tanaka T, Nangaku M. Angiogenesis and hypoxia in the kidney [J]. Nat Rev Nephrol, 2013,9(4) :211-222.
  • 8Hugo C, Daniel C. Thrombospondin in renal disease[ J]. Nephron Exp Nephrol, 2009,111 ( 3 ) : e61456.
  • 9Lu A, Miao M, Schoeb TR, et al. Blockade of TSPl-dependent TGF-β activity reduces renal injury and proteinuria in a murine model of diabetic nephropathy [ J ]. Am J Pathol, 2011,178 ( 6 ) : 2573 -2586.
  • 10Wang S, Lincoln TM, Murphy-Ullrich JE. Glucose downregulation of PKG-I protein mediates increased thrombospondinl-dependent TGF-{beta} activity in vascular smooth muscle cells [ J ]. Am J Physiol Cell Physiol, 2010,298 (5) : C1188-1197.

共引文献4

同被引文献31

引证文献4

二级引证文献28

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部