• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Glutamine and KGF each regulate extracellular thiol/disulfide redox and enhance proliferation in Caco-2 cells.
【24h】

Glutamine and KGF each regulate extracellular thiol/disulfide redox and enhance proliferation in Caco-2 cells.

机译：谷氨酰胺和KGF各自调节细胞外硫醇/二硫键的氧化还原并增强Caco-2细胞的增殖。

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

Glutamine (Gln) and keratinocyte growth factor (KGF) each stimulate intestinal epithelial cell growth, but regulatory mechanisms are not well understood. We determined whether Gln and KGF alter intra- and extracellular thiol/disulfide redox pools in Caco-2 cells cultured in oxidizing or reducing cell medium and whether such redox variations are a determinant of proliferative responses to these agents. Cells were cultured over a physiological range of oxidizing to reducing extracellular thiol/disulfide redox (Eh) conditions, obtained by varying cysteine (Cys) and cystine (CySS) concentrations in cell medium. Cell proliferation was determined by 5-bromo-2-deoxyuridine (BrdU) incorporation. Gln (10 mmol/l) or KGF (10 microg/l) did not alter BrdU incorporation at reducing Eh (-131 to -150 mV), but significantly increased incorporation at more oxidizing Eh (Gln at 0 to -109 mV; KGF at -46 to -80 mV). Cellular glutathione/glutathione disulfide (GSH/GSSG) Eh was unaffected by Gln, KGF, or variations in extracellular Cys/CySS Eh. Control cells largely maintained extracellular Eh at initial values after 24 h (-36 to -136 mV). However, extracellular Eh shifted toward a narrow physiological range with Gln and KGF treatment (Gln -56 to -88 mV and KGF -76 to -92 mV, respectively; P < 0.05 vs. control). The results indicate that thiol/disulfide redox state in the extracellular milieu is an important determinant of Caco-2 cell proliferation induced by Gln and KGF, that this control is independent of intracellular GSH redox status, and that both Gln and KGF enhance the capability of Caco-2 cells to modulate extremes of extracellular redox.
机译：谷氨酰胺（Gln）和角质形成细胞生长因子（KGF）各自刺激肠上皮细胞的生长，但调节机制尚不清楚。我们确定了Gln和KGF是否改变了在氧化或还原细胞培养基中培养的Caco-2细胞中的细胞内和细胞外硫醇/二硫键氧化还原池，以及这种氧化还原变化是否是对这些药物增殖反应的决定因素。通过在改变细胞培养基中半胱氨酸（Cys）和胱氨酸（CySS）浓度获得的氧化至还原细胞外硫醇/二硫化物氧化还原（Eh）条件的生理范围内培养细胞。通过5-溴-2-脱氧尿苷（BrdU）掺入确定细胞增殖。 Gln（10 mmol / l）或KGF（10 microg / l）不会在降低Eh（-131至-150 mV）时改变BrdU的掺入，但是在氧化程度更高的Eh（0至-109 mV时的Gln; KGF）时，掺入量显着增加。在-46至-80 mV时）。细胞谷胱甘肽/谷胱甘肽二硫键（GSH / GSSG）Eh不受Gln，KGF或细胞外Cys / CySS Eh变异的影响。对照细胞在24小时后（-36至-136 mV）在很大程度上将细胞外Eh维持在初始值。然而，通过Gln和KGF治疗，细胞外Eh向狭窄的生理范围移动（分别为Gln -56至-88 mV和KGF -76至-92 mV;与对照组相比，P <0.05）。结果表明，细胞外环境中的巯基/二硫键氧化还原状态是​​由Gln和KGF诱导的Caco-2细胞增殖的重要决定因素，该控制与细胞内GSH氧化还原状态无关，并且Gln和KGF都增强了Gln和KGF的能力。 Caco-2细胞可调节细胞外氧化还原的极限。

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