...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of nephrology. >The role of alpha-smooth muscle actin and platelet-derived growth factor-beta receptor in the progression of renal damage in human IgA nephropathy.
【24h】

The role of alpha-smooth muscle actin and platelet-derived growth factor-beta receptor in the progression of renal damage in human IgA nephropathy.

机译：α平滑肌肌动蛋白和血小板衍生的生长因子β受体在人IgA肾病肾损害进展中的作用。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

BACKGROUND: The degree of tubulointerstitial damage can be considered a better indicator of renal function outcome in IgA nephropathy (N) than the extent of glomerular sclerosis. MATERIALS AND METHODS: To investigate the pathogenetic mechanisms of interstitial injury in IgAN, we used immunohistochemistry and in situ hybridization to evaluate the glomerular and tubolointerstitial expression of PDGF-beta receptor (R) and alpha-smooth muscle actin (SMA), two markers of mesenchymal cell activation, and correlated these findings with the histopathologic and clinical features of the disease. We studied 155 IgAN patients, divided into three groups based on the histological findings (mild, moderate and severe histological lesions). RESULTS: In normal kidneys and in patients with mild histological lesions, the interstitial areas showed scattered peritubular cells positive for PDGF-betaR and alpha-SMA, with a distribution resembling the capillary network. In the glomeruli several cells (mainly in the mesangial area) stained for PDGF-betaR, but only very few cells were positive for alpha-SMA. Alpha-SMA and PDGF-betaR staining, as expected, was also observed in vascular smooth muscle cells. Compared to patients with mild histological lesions, alpha-SMA expression was strikingly increased in patients with moderate to severe lesions, particularly in areas of tubulointerstitial fibrosis. In these patients, PDGF-betaR gene and protein expression, at the tubulointerstitial level, paralleled that in alpha-SMA. Both signals were significantly correlated with the interstitial damage (interstitial infiltrate and fibrosis). Interestingly, these patients showed a different pattern of distribution of alpha-SMA and PDGF-betaR in the glomeruli: PDGF-betaR expression was upregulated, whereas no changes were seen in alpha-SMA staining. In addition, glomerular PDGF-betaR staining was significantly correlated with mesangial cell proliferation, while alpha-SMA was not. Image analysis showed that 40.2+/-10.3/1,000 microm2 of interstitial cells were positive to both PDGF-betaR and alpha-SMA, but only 2.8+/-1.8/1,000 microm of glomerular cells expressed both signals. CONCLUSIONS: Our study supports the hypothesis that interstitial PDGF-betaR and alpha-SMA positive cells may play a key role in the pathogenesis of tubulointerstitial damage.
机译：背景：与肾小球硬化程度相比，肾小管间质损害程度可被视为IgA肾病（N）肾功能预后的更好指标。材料与方法：为了研究IgAN的间质损伤的发病机制，我们使用免疫组织化学和原位杂交技术评估PDGF-β受体（R）和α-平滑肌肌动蛋白（SMA）的肾小球和肾小管间质表达。间充质细胞激活，并将这些发现与疾病的组织病理学和临床特征相关联。我们研究了155例IgAN患者，根据组织学发现（轻度，中度和重度组织学病变）分为三组。结果：在正常肾脏和轻度组织学病变患者中，间质区域显示散在的肾小管周细胞对PDGF-βR和α-SMA呈阳性，分布类似于毛细血管网。在肾小球中，有几个细胞（主要在肾小球膜区）对PDGF-betaR染色，但只有极少数细胞对α-SMA呈阳性。正如预期的那样，在血管平滑肌细胞中也观察到了α-SMA和PDGF-βR染色。与具有轻度组织学病变的患者相比，在具有中度至重度病变的患者中，尤其是在肾小管间质纤维化区域，α-SMA表达显着增加。在这些患者中，肾小管间质水平的PDGF-betaR基因和蛋白质表达与α-SMA相似。两种信号均与间质损害（间质浸润和纤维化）显着相关。有趣的是，这些患者肾小球中的α-SMA和PDGF-betaR分布不同：PDGF-betaR表达上调，而α-SMA染色未见变化。另外，肾小球PDGF-βR染色与系膜细胞增殖显着相关，而α-SMA则不相关。图像分析显示，间质细胞的40.2 +/- 10.3 / 1,000 microm2对PDGF-betaR和α-SMA均呈阳性，但只有2.8 +/- 1.8 / 1,000 microm的肾小球细胞表达两种信号。结论：我们的研究支持间质性PDGF-βR和α-SMA阳性细胞可能在肾小管间质性损伤的发病机制中起关键作用的假说。

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