...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Cell and Tissue Research >Increased cardiac remodeling in cardiac-specific Flt-1 receptor knockout mice with pressure overload
【24h】

Increased cardiac remodeling in cardiac-specific Flt-1 receptor knockout mice with pressure overload

机译：压力超负荷的心脏特异性Flt-1受体敲除小鼠的心脏重塑增加

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

Vascular endothelial growth factor (VEGF) inhibition has previously been shown to have damaging effects on the heart. Because the role of Flt-1 (a phosphotyrosine kinase receptor for VEGF) in cardiac function and hypertrophy is unclear, we generated mice lacking Flt-1 only in their cardiomyocytes (Flt-1 KO). The hearts from 8- to 10-week-old mice were measured by using echocardiography and histology. No significant differences were seen in fraction shortening, cross-sectional area of cardiomyocytes, and interstitial collagen fraction between littermate controls and KO mice at baseline. To test the hypothesis that Flt-1 is involved in cardiac remodeling, we performed transverse aorta constriction (TAC) by ligating the transverse ascending aorta. Four weeks after TAC, echocardiography of the mice was performed, and the hearts were excised for pathological analysis and Western blotting. No difference in mortality was found between Flt-1 KO mice and controls; however, KO mice showed a greater cardiomyocyte cross-sectional area and interstitial collagen fraction than controls. Western blotting indicated that AKT was activated less in Flt-1 KO hearts after TAC compared with that in control hearts. Thus, Flt-1 deletion in cardiomyocytes increased hypertrophy, fibrosis, and regression of AKT phosphorylation. Our study suggests that Flt-1 plays a critical role in cardiac hypertrophy induced by pressure overload via the activation of AKT, which seems to be cardioprotective.
机译：血管内皮生长因子（VEGF）抑制作用先前已显示对心脏有破坏作用。由于尚不清楚Flt-1（VEGF的磷酸酪氨酸激酶受体）在心脏功能和肥大中的作用，因此我们生成了仅在其心肌细胞（Flt-1 KO）中缺少Flt-1的小鼠。使用超声心动图和组织学方法测量8至10周龄小鼠的心脏。在基线时，同窝对照和KO小鼠之间在缩短分数，心肌细胞的横截面积和间质胶原分数方面没有观察到显着差异。为了检验Flt-1参与心脏重塑的假说，我们通过结扎横向升主动脉进行了横向主动脉缩窄（TAC）。 TAC后四周，对小鼠进行超声心动图检查，并切除心脏进行病理分析和蛋白质印迹。在Flt-1 KO小鼠和对照组之间未发现死亡率差异。然而，KO小鼠显示出比对照组更大的心肌横截面积和间质胶原分数。 Western blotting显示，TAC后Flt-1 KO心脏中的AKT活化程度低于对照组心脏。因此，心肌细胞中Flt-1的缺失会增加肥大，纤维化和AKT磷酸化的退化。我们的研究表明Flt-1在通过AKT激活而引起的压力超负荷所致的心肌肥大中起关键作用，而AKT似乎具有心脏保护作用。

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