...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Contributions of Rho-kinase and AMP-related kinase signaling pathways to responses mediated by endothelium-derived contracting factors in diabetic rat aorta
【24h】

Contributions of Rho-kinase and AMP-related kinase signaling pathways to responses mediated by endothelium-derived contracting factors in diabetic rat aorta

机译：RHO-激酶和AMP相关激酶信号传导途径对糖尿病大鼠主动脉内皮衍生的收缩因子介导的反应的贡献

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

Diabetes-induced endothelial damage leads to vascular dysfunction. The current study investigated the effects of short-term (4-week) streptozotocin (STZ)-induced diabetes on responses mediated by endothelium-derived contracting factors (EDCFs) as well as possible contributions of Rho-kinase and AMP-activated kinase (AMPK) signaling pathways. The effects of STZ-diabetes on vascular function were examined in isolated thoracic aorta preparations of 30-week-old rats (n = 27). The diabetes-associated changes in vascular function were studied with calcium ionophore A23187, acetylcholine, Rho-kinase inhibitor Y27632 ((R)-(+)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride), and AMPK activator AICAR (5-aminoimidazole-4- carboxamide-1-beta-D-ribofuranoside). The phosphorylation of acetyl-CoA carboxylase, AMPK, and phospholamban and the protein levels of sarcoplasmic/endoplasmic Ca2+-ATPase 2 (SERCA2) and Rho-associated protein kinase (ROCKII) were measured in aortic preparations. Although the acetylcholine-mediated relaxation responses were preserved in 4-week STZ-induced diabetes, the increased activation of the Rho-kinase pathway was demonstrated via twofold enhancement in A23187-mediated contractile responses and significantly augmented protein levels of ROCKII. The AICAR-activated AMPK-mediated relaxation response was also augmented similar to 4-fold in diabetic rats, without any alteration in phospholamban phosphorylation; further, this relaxation response suppressed A23187-mediated contraction in both groups. Diabetic rats showed an increase in AICAR-induced AMPK-mediated vasorelaxation and a 2.5-fold elevation of phosphorylated AMPK levels. These results indicate a possible compensation between hyperglycemia-induced endothelium-dependent hypercontractility and AMPK-mediated vasorelaxation in diabetes.
机译：糖尿病诱导的内皮损伤导致血管功能障碍。目前的研究调查了短期（4周）链脲佐菌素（STZ）诱导的糖尿病对内皮衍生的收缩因子（EDCFS）介导的反应的影响以及RHO-激酶和AMP-活化激酶的可能贡献（AMPK ）信号传导途径。在30周龄大鼠的孤立胸主动脉制剂中检测了STZ-糖尿病对血管功能的影响（n = 27）。用钙离子载体A23187，乙酰胆碱，rhO-激酶抑制剂Y27632（（R） - （+） - 反式-4-（1-氨基乙基）-N-（4-吡啶基）环己烷酰甲酰胺二盐酸钙，研究了血管功能的糖尿病相关变化）和AMPK活化剂AICAR（5-氨基咪唑-4-甲酰胺-1-Beta-D-核苷酸）。在主动脉制剂中测量乙酰-CoA羧化酶，AMPK和磷蛋白的磷酸化和磷酰胺蛋白酶的磷酸盐/内质Ca2 + -AtPase 2（Serca2）和Rho相关蛋白激酶（ROVO-相关蛋白激酶（ROVIII）的磷酸化。虽然在4周的STZ诱导的糖尿病中保留了乙酰胆碱介导的弛豫响应，但是通过双重增强的A23187介导的收缩响应和显着增强的岩石蛋白水平，通过双重增强来证明RHO-激酶途径的增加。 AICAR活化的AMPK介导的弛豫响应也增强了糖尿病大鼠中的4倍，没有磷酰胺磷酸化的任何改变;此外，这种弛豫响应抑制了两组中的A23187介导的收缩。糖尿病大鼠表现出AiCar诱导的AMPK介导的血管内升压和2.5倍的磷酸化AMPK水平的升高。这些结果表明高血糖诱导的内皮依赖性血密分构和AMPK介导的糖尿病患者的可能补偿。

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