• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cytokine >Inflammation triggers high mobility group box 1 (HMGB1) secretion in adipose tissue, a potential link to obesity
【24h】

Inflammation triggers high mobility group box 1 (HMGB1) secretion in adipose tissue, a potential link to obesity

机译：炎症触发脂肪组织中高迁移率族1（HMGB1）的分泌，这可能与肥胖有关

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: Low grade inflammation is one of the major metabolic disorders in case of obesity due to variable secretion of adipose derived cytokines called adipokines. Recently the nuclear protein HMGB1 was identified as an inflammatory alarmin in obesity associated diseases. However HMGB1 role in adipose tissue inflammation is not yet studied. Objectives: The aim of this study was to prove the expression of HMGB1 in human adipose tissue and to assess the levels of expression between normo-weight and obese individuals. Furthermore we determined which type of cells within adipose tissue is involved in HMGB1 production under inflammatory signal. Methods: Western-blot was performed on protein lysates from human normo-weight and obese adipose tissue to study the differential HMGB1 expression. Human normo-weight adipose tissue, adipose-derived stromal cells (ASCs) and adipocytes were cultured and stimulated with LPS to induce inflammation. HMGB1, IL-6 and MCP-1 secretion and gene expression were quantified by ELISA and Q-PCR respectively, as well as cell death by LDH assay. HMGB1 translocation during inflammation was tracked down by immunofluorescence in ASCs. Results: HMGB1 was expressed 2-fold more in adipose tissue from obese compared to normo-weight individuals. LPS led to an up-regulation in HMGB1 secretion and gene expression in ASCs, while no change was noticed in adipocytes. Moreover, this HMGB1 release was not attributable to any cell death. In LPS-stimulated ASCs, HMGB1 translocation from nucleus to cytoplasm was detectable at 12. h and the nuclear HMGB1 was completely drained out after 24. h of treatment. Conclusion: The expression level studies between adipose tissue from normo-weight and obese individuals together with in vitro results strongly suggest that adipose tissue secretes HMGB1 in response to inflammatory signals which characterized obesity.
机译：背景：在肥胖的情况下，低级炎症是主要的新陈代谢疾病之一，这是由于脂肪衍生的称为脂肪因子的细胞因子的分泌不同而引起的。最近，核蛋白HMGB1被鉴定为肥胖相关疾病中的一种炎症警报素。但是，尚未研究HMGB1在脂肪组织炎症中的作用。目的：本研究的目的是证明HMGB1在人体脂肪组织中的表达，并评估正常体重和肥胖个体之间的表达水平。此外，我们确定了在炎症信号下脂肪组织中哪些细胞类型参与HMGB1的产生。方法：对人体正常体重和肥胖脂肪组织的蛋白裂解物进行蛋白质印迹分析，以研究HMGB1的差异表达。培养人正常体重的脂肪组织，脂肪来源的基质细胞（ASC）和脂肪细胞，并用LPS刺激以诱导炎症。分别通过ELISA和Q-PCR对HMGB1，IL-6和MCP-1的分泌和基因表达进行定量，并通过LDH测定对细胞的死亡进行定量。通过ASC中的免疫荧光可以追踪炎症过程中的HMGB1转运。结果：与正常体重的个体相比，肥胖的脂肪组织中HMGB1的表达高2倍。 LPS导致ASC中HMGB1分泌和基因表达上调，而脂肪细胞中未发现变化。此外，此HMGB1释放不归因于任何细胞死亡。在LPS刺激的ASC中，在12 h时可检测到HMGB1从细胞核到细胞质的转运，并且在处理24 h后，HMGB1的核被完全排出。结论：正常体重和肥胖个体的脂肪组织之间的表达水平研究以及体外结果强烈表明，脂肪组织响应于表征肥胖的炎性信号而分泌HMGB1。

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