...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell and Tissue Research >Three-dimensional culture model for analyzing crosstalk between adipose tissue and hepatocytes
【24h】

Three-dimensional culture model for analyzing crosstalk between adipose tissue and hepatocytes

机译：用于分析脂肪组织与肝细胞之间串扰的三维培养模型

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

Systemic adipose tissue is involved in the pathophysiology of obesity-associated liver diseases. However, a method has not been established for analyzing the direct interaction between adipose tissue and hepatocytes. We describe a useful three-dimensional model comprising a collagen gel coculture system in which HepG2 hepatocytes are cultured on a gel layer with visceral adipose tissue fragments (VAT) or subcutaneous tissue samples (SAT). Male adipose tissues were obtained from 5-week-old Wistar rats and human autopsy cases. Cellular behavior was analyzed by electron microscopy, immunohistochemistry, Western blot, real-time reverse transcription plus the polymerase chain reaction and enzyme-linked immunosorbent assay. VAT significantly promoted lipid accumulation and apoptosis in HepG2 cells and suppressed their growth and differentiation compared with SAT. VAT produced higher concentrations of fatty acids (palmitate, oleate, linoleate) than SAT. HepG2 cells significantly decreased the production of these fatty acids in VAT. Only HepG2 cells treated with 250 μM palmitate replicated VAT-induced apoptosis. Neither VAT nor SAT affected lipotoxicity-associated signals of nuclear factor kappa B, c-Jun N-terminal kinase and inositol requiring enzyme-1α in HepG2 cells. HepG2 cells never affected adiponectin, leptin, or resistin production in VAT and SAT. The data indicate that our model actively creates adipose tissue and HepG2 hepatocyte interactions, suggesting that (1) VAT plays more critical roles in hepatocyte lipotoxicity than SAT; (2) palmitate but not adipokines, is partly involved in the mechanisms of VAT-induced lipotoxicity; (3) HepG2 cells might inhibit fatty acid production in VAT to protect themselves against lipotoxicity. Our model should serve in studies of interactions between adipose tissue and hepatocytes and of the mechanisms in obesity-related lipotoxicity and liver diseases.
机译：全身脂肪组织参与与肥胖相关的肝病的病理生理。但是，尚未建立分析脂肪组织与肝细胞之间直接相互作用的方法。我们描述了一个有用的三维模型，其中包括胶原凝胶共培养系统，其中HepG2肝细胞与内脏脂肪组织片段（VAT）或皮下组织样本（SAT）一起在凝胶层上培养。雄性脂肪组织取自5周龄的Wistar大鼠和人体解剖病例。通过电子显微镜，免疫组织化学，蛋白质印迹，实时逆转录加上聚合酶链反应和酶联免疫吸附测定法分析细胞行为。与SAT相比，增值税可显着促进HepG2细胞中脂质的积累和凋亡，并抑制其生长和分化。与SAT相比，增值税产生的脂肪酸（棕榈酸，油酸，亚油酸）浓度更高。 HepG2细胞显着降低了增值税中这些脂肪酸的产生。仅用250μM棕榈酸酯处理的HepG2细胞复制了VAT诱导的凋亡。 VAT和SAT均不影响HepG2细胞中需要酶1α的核因子kappa B，c-Jun N端激酶和肌醇的脂毒性相关信号。 HepG2细胞从未影响过VAT和SAT中的脂联素，瘦素或抵抗素的产生。数据表明，我们的模型积极地建立了脂肪组织和HepG2肝细胞的相互作用，这表明（1）增值税在肝细胞脂毒性中的作用比SAT更重要; （2）棕榈酸酯而不是脂肪因子，部分参与了增值税诱发的脂毒性机制; （3）HepG2细胞可能会抑制增值税中的脂肪酸产生，从而保护自己免受脂毒性。我们的模型应用于研究脂肪组织与肝细胞之间的相互作用以及肥胖相关的脂毒性和肝脏疾病的机制。

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