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首页> 外文期刊>Pathobiology: journal of immunopathology, molecular and cellular biology >Spatial and phenotypic characterization of vascular remodeling in a mouse model of asthma.
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Spatial and phenotypic characterization of vascular remodeling in a mouse model of asthma.

机译：哮喘小鼠模型中血管重塑的空间和表型特征。

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Asthma is a chronic inflammatory disease characterized by airway wall remodeling in which vascular remodeling is thought to be a main contributor. Vascular endothelial growth factor (VEGF) is known as a major regulator of angiogenesis and enhancer of vascular permeability. Here, we define the spatial nature of vascular remodeling and the role of VEGF and its receptors (Flt-1 and Flk-1) in the allergic response in mice (A/J) susceptible to the development of allergen-induced airway hyperresponsiveness using morphometric and quantitative approaches. Increased vascularity, vasodilatation, and endothelial cell proliferation were found in the tracheal and bronchial walls in the early and late phases of asthma. Vascular changes were observed not only in small vessels but also in larger vessels. In contrast to normal control, lung tissue from the asthma model showed dual expression for CD31 and von Willebrand factor in the endothelial cells and alpha-smooth muscle actin and desmin in the mural cells of the vessels, suggesting a phenotypic and functional transformation. The mRNA levels of VEGF isoforms, VEGF(164) and VEGF(188), were significantly increased in the tracheal and lung tissue, respectively. In addition, the mRNA level of VEGF receptor Flk-1 was significantly increased in the trachea. These results establish the existence of vascular remodeling in the airways in a mouse model of allergic asthma and support a key role for the expression of unique VEGF isoform genes as mediators of structural changes.
机译：哮喘是一种慢性炎症性疾病，其特征是气道壁重塑，其中血管重塑被认为是主要的病因。血管内皮生长因子（VEGF）被称为血管生成的主要调节剂和血管通透性的增强剂。在这里，我们定义了血管重塑的空间性质以及VEGF及其受体（Flt-1和Flk-1）在易受变应原诱导气道高反应性发展的小鼠（A / J）的过敏反应中的作用，使用形态计量学和定量方法。在哮喘的早期和晚期，在气管壁和支气管壁中发现血管，血管舒张和内皮细胞增殖增加。不仅在小血管中观察到血管变化，而且在大血管中也观察到。与正常对照相比，哮喘模型的肺组织在血管内皮细胞中表达CD31和von Willebrand因子，在血管壁细胞中表达α-平滑肌肌动蛋白和结蛋白，提示其表型和功能转变。在气管和肺组织中，VEGF亚型，VEGF（164）和VEGF（188）的mRNA水平显着升高。另外，气管中VEGF受体Flk-1的mRNA水平显着增加。这些结果建立了过敏性哮喘小鼠模型中气道中血管重塑的存在，并支持表达独特的VEGF同工型基因作为结构改变的介质的关键作用。

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