• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>American Journal of Physiology >Insulin resistance does not diminish eNOS expression, phosphorylation, or binding to HSP-90.
【24h】

Insulin resistance does not diminish eNOS expression, phosphorylation, or binding to HSP-90.

机译：胰岛素抵抗不会减弱eNOS的表达，磷酸化或与HSP-90的结合。

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

Previously, using an animal model of syndrome X, the obese Zucker rat (OZR), we documented impaired endothelium-dependent vasodilation. The aim of this study was to determine whether reduced expression or altered posttranslational regulation of endothelial nitric oxide synthase (eNOS) underlies the vascular dysfunction in OZR rats. There was no significant difference in the relative abundance of eNOS in hearts, aortas, or skeletal muscle between lean Zucker rats (LZR) and OZR regardless of age. There was no difference in eNOS mRNA levels, as determined by real-time PCR, between LZR and OZR. The inability of insulin resistance to modulate eNOS expression was also documented in two additional in vivo models, the ob/ob mouse and the fructose-fed rat, and in vitro via adenoviral expression of protein tyrosine phosphatase 1B in endothelial cells. We next investigated whether changes in the acute posttranslational regulation of eNOS occurs with insulin resistance. Phosphorylation of eNOS at S632 (human S633)and T494 was not different between LZR and OZR; however, phosphorylation of S1176 was significantly enhanced in OZR. Phosphorylation of S1176 was not different in the ob/ob mouse or in fructose-fed rats. The association of heat shock protein 90 with eNOS, a key regulatory step controlling nitric oxide and aberrant O2- production, was not different between OZR and LZR. Taken together, these results suggest that changes in eNOS expression or posttranslation regulation do not underlie the vascular dysfunction seen with insulin resistance and that other mechanisms, such as altered localization, reduced availability of cofactors, substrates, and the elevated production of O2-, may be responsible.
机译：以前，使用X综合征动物模型（肥胖的Zucker大鼠（OZR）），我们记录了内皮依赖性血管舒张功能受损。这项研究的目的是确定内皮一氧化氮合酶（eNOS）的表达降低或翻译后调节的改变是否是OZR大鼠血管功能障碍的基础。无论年龄大小，瘦Zucker大鼠（LZR）和OZR在心脏，主动脉或骨骼肌中的eNOS相对丰度均无显着差异。通过实时PCR测定，LZR和OZR之间的eNOS mRNA水平没有差异。还通过另外两个体内模型（ob / ob小鼠和果糖喂养的大鼠）以及体外通过内皮细胞中蛋白酪氨酸磷酸酶1B的腺病毒表达，证明了胰岛素抵抗无法调节eNOS表达。接下来，我们调查了胰岛素抵抗对eNOS的急性翻译后调节的影响是否发生。 LZR和OZR之间eNOS在S632（人S633）和T494的磷酸化没有差异。然而，在OZR中S1176的磷酸化显着增强。在ob / ob小鼠或果糖喂养的大鼠中，S1176的磷酸化没有差异。在OZR和LZR之间，热休克蛋白90与eNOS（控制一氧化氮和异常O2产生的关键调控步骤）之间的关联没有差异。综上所述，这些结果表明，eNOS表达的变化或翻译后调节并不构成胰岛素抵抗所见的血管功能障碍，其他机制，例如改变的定位，辅助因子，底物的可用性降低以及O2-的生成可能增加要负责任。

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