• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >TGF-beta1 induces IL-8 and MCP-1 through a connective tissue growth factor-independent pathway.
【24h】

TGF-beta1 induces IL-8 and MCP-1 through a connective tissue growth factor-independent pathway.

机译：TGF-beta1通过结缔组织生长因子非依赖性途径诱导IL-8和MCP-1。

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

Transforming growth factor-beta(1) (TGF-beta(1)) functions as an important immunomodulatory cytokine in human kidney. Evidence suggests that connective tissue growth factor (CTGF) is an important downstream mediator of the profibrotic effects of TGF-beta(1). However, the role of CTGF in TGF-beta(1)-induced chemokine production remains unknown. This study was undertaken to determine whether CTGF is involved in mediating TGF-beta(1)-induced chemokine production in renal proximal tubular (HK-2) cells. Interleukin-8 (IL-8) and macrophage chemoattractant protein-1 (MCP-1) were measured. TGF-beta(1) induced an increase in IL-8 and MCP-1 (both P < 0.05) compared with control levels. CTGF was effectively silenced using small interference RNA (siRNA) in HK-2 cells. RT-PCR and real-time PCR confirmed a 94% reduction in CTGF mRNA. In the CTGF-silenced cells, TGF-beta(1)-stimulated IL-8 and MCP-1 secretion was not altered compared with control cells. Similarly, basal secretion of IL-8 and MCP-1 was not changed in CTGF-silenced cells. The direct effect of CTGF (20, 200, and 400 ng/ml) on IL-8 and MCP-1 was assessed at 24-, 48-, and 72-h time points and no stimulation was observed. Our studies further demonstrate that in the CTGF gene-silenced cells, CTGF partially mediates TGF-beta(1)-induced fibronectin and collagen IV secretion. These data suggest that TGF-beta(1) induced IL-8 and MCP-1 via CTGF-independent pathway. TGF-beta mediates both fibrosis and chemokine production in the proximal tubule of the kidney. However, CTGF plays a more specific role as a downstream mediator of TGF-beta(1)-induced fibrosis.
机译：转化生长因子-β（1）（TGF-β（1））在人肾脏中起着重要的免疫调节细胞因子的作用。有证据表明，结缔组织生长因子（CTGF）是TGF-beta（1）的纤维化作用的重要下游介质。但是，CTGF在TGF-β（1）诱导的趋化因子生产中的作用仍然未知。进行这项研究以确定CTGF是否参与介导TGF-β（1）诱导的肾近端肾小管（HK-2）细胞趋化因子的产生。测量白细胞介素8（IL-8）和巨噬细胞趋化蛋白-1（MCP-1）。与对照组相比，TGF-β（1）诱导了IL-8和MCP-1的增加（均P <0.05）。使用HK-2细胞中的小干扰RNA（siRNA）可有效沉默CTGF。 RT-PCR和实时PCR证实CTGF mRNA降低了94％。在CTGF沉默的细胞中，与对照细胞相比，TGF-β（1）刺激的IL-8和MCP-1分泌没有改变。同样，在CTGF沉默的细胞中，IL-8和MCP-1的基础分泌没有改变。在24、48和72小时的时间点评估了CTGF（20、200和400 ng / ml）对IL-8和MCP-1的直接作用，未观察到刺激。我们的研究进一步证明，在CTGF基因沉默的细胞中，CTGF部分介导TGF-beta（1）诱导的纤连蛋白和胶原IV分泌。这些数据表明TGF-beta（1）通过CTGF依赖性途径诱导IL-8和MCP-1。 TGF-β介导肾脏近端小管中的纤维化和趋化因子的产生。但是，CTGF作为TGF-beta（1）诱导的纤维化的下游介质起着更具体的作用。

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