ABSTRACT

A decrease in oxygen concentration is a hallmark of inflammatory reactions resulting from infection or homeostasis disorders. Mast cells interact with extracellular matrix and other cells by adhesion receptors. We investigated the effect of hypoxia on integrin-mediated mast cell adhesion to fibronectin. We found that it was mediated by the α5/β1 receptor and that hypoxia significantly upregulated this process. Hypoxia-mediated increases in mast cell adhesion occurred without increased surface expression of integrins, suggesting regulation by inside-out integrin signaling. Hypoxia also mediated an increase in phosphorylation of Akt, and PI3’kinase inhibitors abolished hypoxia-mediated mast cell adhesion. Hypoxia upregulates the function of integrin receptors by PI3’ kinase-dependent signaling. This process might be important for the location of mast cells at inflammatory sites

摘要

氧气浓度的降低是感染或体内稳态疾病引起的炎症反应的标志。肥大细胞通过粘附受体与细胞外基质和其他细胞相互作用。我们研究了缺氧对整联蛋白介导的肥大细胞对纤连蛋白粘附的影响。我们发现它是由α5/β1受体介导的，缺氧显着上调了该过程。缺氧介导的肥大细胞粘附增加没有增加整联蛋白的表面表达，表明由内而外的整联蛋白信号调节。低氧还介导了Akt磷酸化的增加，而PI3'激酶抑制剂则消除了低氧介导的肥大细胞粘附。缺氧通过PI3'激酶依赖性信号转导整联蛋白受体的功能。