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Temporal changes of angiopoietins and Tie2 expression in rat lungs after monocrotaline-induced pulmonary hypertension

机译:克豆肾上腺素诱发的肺动脉高压后大鼠肺中血管生成素和Tie2表达的时间变化。

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Angiogenic factors such as vascular endothelial growth factor (VEGF) are implicated in pulmonary hypertension (PH). However, the pathway of angiogenic factor-mediated pathologic angiogenesis in PH remains unclear. In this study, we evaluated the temporal expression of angiopoietin (Ang) 1, Ang2, and their receptor (Tie2) as well as VEGF, endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and heme oxygenase 1 (HO1) in the monocrotaline-induced PH model. Histologic evaluation showed pathologic vascular remodeling in the arteries of lung sections 1 wk after monocrotaline treatment. Protein levels of Ang1, Ang2, eNOS, iNOS, HO1, and VEGF were increased 1 wk after monocrotaline treatment but Tie2 protein levels were decreased 2 wk afterward. These results suggest that Ang2 mediates vascular remodeling in PH by decreasing Tie2 expression. Therefore, the Ang-Tie2 system may play a role in the pathophysiology of PH.
机译:血管生成因子,例如血管内皮生长因子(VEGF)与肺动脉高压(PH)有关。然而,PH中血管生成因子介导的病理性血管生成的途径仍不清楚。在这项研究中,我们评估了血管生成素(Ang)1,Ang2及其受体(Tie2)以及VEGF,内皮型一氧化氮合酶(eNOS),诱导型NOS(iNOS)和血红素加氧酶1(HO1)的时间表达。在单芥子碱诱导的PH模型中。组织学评估显示,在单肾上腺素治疗后1周,肺部动脉的病理性血管重塑。单crocrotaline处理后1周,Ang1,Ang2,eNOS,iNOS,HO1和VEGF的蛋白水平升高,但随后2周,Tie2蛋白水平降低。这些结果表明Ang2通过降低Tie2表达来介导PH的血管重塑。因此,Ang-Tie2系统可能在PH的病理生理中起作用。

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