• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cellular Physiology and Biochemistry >Expression of the serine/threonine kinase hSGK1 in chronic viral hepatitis
【24h】

Expression of the serine/threonine kinase hSGK1 in chronic viral hepatitis

机译：丝氨酸/苏氨酸激酶hSGK1在慢性病毒性肝炎中的表达

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

The human serine/threonine kinase hSGK1 is expressed ubiquitously with highest transcript levels in pancreas and liver. This study has been performed to determine the hSGK1 distribution in normal liver and its putative role in fibrosing liver disease. HSGK1-localization was determined by in situ hybridization, regulation of hSGK1-transcription by Northern blotting, fibronectin synthesis and hSGK1 phosphorylation by Western blotting. In normal liver hSGK1 was mainly transcribed by Kupffer cells. In liver tissue from patients with chronic viral hepatitis, hSGK1 transcript levels were excessively high in numerous activated Kupffer cells and inflammatory cells localized within fibrous septum formations. HSGK1 transcripts were also detected in activated hepatic stellate cells. Accordingly, Western blotting revealed that tissue from fibrotic liver expresses excessive hSGK1 protein as compared to normal liver. TGF-beta1 (2 ng/ml) increases hSGK1 transcription in both human U937 macrophages and HepG2 hepatoma cells. H2O2 (0.3 mM) activated hSGK1 and increased fibronectin formation in HepG2 cells overexpressing hSGK1 but not in HepG2 cells expressing the inactive mutant hSGK1(K127R). In conclusion hSGK1 is upregulated by TGF-beta1 during hepatitis and may contribute to enhanced matrix formation during fibrosing liver disease. Copyright (C) 2002 S. Karger AG, Basel. [References: 37]
机译：人丝氨酸/苏氨酸激酶hSGK1在胰腺和肝脏中以最高的转录水平普遍表达。已经进行了这项研究以确定hSGK1在正常肝脏中的分布及其在肝纤维化疾病中的假定作用。 HSGK1定位通过原位杂交，Northern印迹调节hSGK1转录，纤连蛋白合成和Western印迹确定hSGK1磷酸化来确定。在正常肝脏中，hSGK1主要由库普弗细胞转录。在患有慢性病毒性肝炎的患者的肝组织中，hSGK1转录水平在许多活化的库普弗细胞和位于纤维间隔形成中的炎性细胞中过高。在活化的肝星状细胞中也检测到HSGK1转录本。因此，蛋白质印迹显示与正常肝脏相比，来自纤维化肝脏的组织表达过量的hSGK1蛋白。 TGF-beta1（2 ng / ml）在人U937巨噬细胞和HepG2肝癌细胞中均增加hSGK1转录。 H2O2（0.3 mM）在过表达hSGK1的HepG2细胞中激活hSGK1，并增加纤连蛋白的形成，但在表达无活性突变型hSGK1（K127R）的HepG2细胞中则没有。总之，hSGK1在肝炎期间被TGF-beta1上调，并可能在纤维化肝病期间促进基质形成。版权所有（C）2002 S.Karger AG，巴塞尔。 [参考：37]

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