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原发性局灶节段性肾小球硬化的转录组学研究 被引量:1

The transcriptomic analysis in primary focal segmental glomerulosclerosis
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摘要 转录组学是从RNA水平研究基因表达情况的学科。目前用于转录组数据获得和分析的方法主要有基于杂交技术的生物芯片技术和基于测序的RNA测序技术,这些方法的出现使得对细胞、组织表达谱的高通量分析成为可能,通过这些方法可以获得许多与疾病相关信息。原发性局灶节段性肾小球硬化(FSGS)是导致成人及儿童激素抵抗肾病综合征和肾衰竭的最常见原因之一,其病理生理机制至今仍不清楚。因此,有必要对其发病机制进行深入研究。近年来,数项FSGS的转录组学研究结果相继发表,进一步了解FSGS的致病机制提供了重要信息,本文就其在FSGS中的发现做一综述。 Transcriptomics is an approach to study gene expression change based on RNA level. Currently, there are mainly two technologies used for collecting and analyzing transcriptomic data, i,e., microarray that is based on nucleic acid molecular hybridization, and RNA sequencing (RNA-Seq) based on direct sequencing to identify the RNA molecules. Both of the two technologies have made high throughput gene expression profiling of cells and tissues available, and they have provided insights into the mechanisms of various diseases, Focal segmental glomerulosclerosis (FSGS) is one of the most common causes of steroid resistant nephrotic syndrome (SRNS) and renal failure among adults and children. The pathomechanism of FSGS is still unclear, and further effort is required to understand this disease. There have been several studies in which transcriptomic analysis of FSGS were performed, which have provided some insights into the mechanism of FSGS. This review describes the findings in these studies.
作者 仝君 陈楠
出处 《肾脏病与透析肾移植杂志》 CAS CSCD 北大核心 2014年第4期360-367,共8页 Chinese Journal of Nephrology,Dialysis & Transplantation
基金 国家重点基础研究发展计划(2012CB517604) 国家自然科学基金(81370015)
关键词 原发性局灶节段性肾小球硬化 转录组学 生物芯片技术 RNA测序技术 primary focal segmental glomerulosclerosis transcriptome Microarray RNA Sequencing
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  • 1Remuzzi G, Bertani T. Pathophysiology of progressive nephropathies. N Engl J Med 1998; 339: 1448-56.
  • 2Baricos WH, Cortez SL, el-Dahr SS, Schnaper HW. ECM degradation by cultured human mesangial cells is mediated by a PA/plasmin/ MMP-2 cascade. Kidney Int 1995; 47:1039-47
  • 3Eddy AA. Plasminogen activator inhibitor-1 and the kidney. Am J Physiol Renal Physiol 2002; 283: F209-20.
  • 4Matsuo S, Lopez-Guisa JM, Cai X, Okamura DM, Alpers CE, Bumgarner RE, et al. Multifunctionality of PAI-1 in fibrogenesis: evidence from obstructive nephropathy in PAI-1-overexpressing mice. Kidney Int 2005; 67: 2221-38.
  • 5Oda T, Jung YO, Kim HS, Cai X, Lopez-Guisa JM, Ikeda Y, et al. PAI-1 deficiency attenuates the fibrogenic response to ureteral obstruction. Kidney Int 2001; 60: 587-96.
  • 6Nicholas SB, Aguiniga E, Ren Y, Kim J, Wong J, Govindarajan N, et al. Plasminogen activator inhibitor-1 deficiency retards diabetic nephropathy. Kidney lnt 2005; 67: 1297-307.
  • 7Krag S, Danielsen CC, Carmeliet P, Nyengaard J, Wogensen L. Plasminogen activator inhibitor-1 gene deficiency attenuates TGF-betal- induced kidney disease. Kidney Int 2005; 68: 2651-66.
  • 8Huang Y, Haraguchi M, Lawrence DA, Border WA, Yu L, Noble NA. A mutant, noninhibitory plasminogen activator inhibitor type 1 decreases matrix accumulation in experimental glomerulonephritis. J Clin Invest 2003; 112: 379-88.
  • 9Huang Y, Border WA, Lawrence DA, Noble NA. Noninhibitory PAI-1 enhances plasmin-mediated matrix degradation both in vitro and in experimental nephritis. Kidney Int 2006; 70: 515-22.
  • 10Schnaper HW, Hayashida T, Hubchak SC, Poncelet AC. TGF-beta signal transduction and mesangial cell fibrogenesis. Am J Physiol Renal Physiol 2003; 284: F243-52.

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