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Effects of hypoxia and hypercapnia on surfactant protein expression proliferation and apoptosis in A549 alveolar epithelial cells

机译：低氧和高碳酸血症对肺泡上皮细胞A549表面蛋白表达增殖和凋亡的影响

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摘要

During lung injury alveolar epithelial cells are directly exposed to changes in PO2 and PCO2. Integrity of alveolar epithelial type 11 cells (AECII) is critical in lung injury but the effect of hypoxia and hypercapnia on AECII function, viability and proliferation has not been clearly investigated. Aim of the present work was to determine the direct effect of hypoxia and hypercapnia on surfactant protein expression, proliferation and apoptosis of lung epithelial cells in vitro. A549 alveolar epithelia cells were subjected to hypoxia (1%O-2-5% CO2) or hypercapnia (21% O-2-15% CO2) and expression of surfactant protein C was measured and compared to normal conditions (21% O-2- 5% CO2). Cell cycle progression and apoptosis were measured by flow cytometric analysis. Results: A549 alveolar epithelial cells produce surfactant proteins, including surfactant protein C, when cultured under normal conditions, which is reduced under hypoxic conditions. Specifically, pro-SpC expression is moderately decreased after 8 h of culture in hypoxia, and is completely attenuated after 48 h. Hypercapnia decreases pro-SpC expression only after 48 h of exposure. Stimulation with TNF-alpha partly reverses pSPC decrease observed under hypoxic and hypercapnic conditions. Hypoxic culture of A549 cells results in progressive arrest of cells in the G1 phase of the cell cycle and increased apoptosis first observed 4 h following exposure and peaking at 24 h. In contrast hypercapnia has no significant effect on alveolar epithelial cell proliferation or apoptosis. Conclusions: Taken together we can conclude that hypoxia rapidly and severely affects AECII function and viability while hypercapnia has an inhibitory effect on pro-SpC production only after prolonged exposure.
机译：在肺损伤期间，肺泡上皮细胞直接暴露于PO2和PCO2的变化。肺泡上皮11型细胞（AECII）的完整性在肺部损伤中至关重要，但缺氧和高碳酸血症对AECII功能，生存力和增殖的影响尚未明确研究。本研究的目的是确定缺氧和高碳酸血症对肺上皮细胞表面活性剂蛋白表达，增殖和凋亡的直接影响。对A549肺泡上皮细胞进行低氧（1％O-2-5％CO2）或高碳酸血症（21％O-2-15％CO2），测量表面活性剂蛋白C的表达并将其与正常条件（21％O- 2-5％的二氧化碳）。通过流式细胞术分析测量细胞周期进程和凋亡。结果：在正常条件下培养时，A549肺泡上皮细胞产生表面活性剂蛋白，包括表面活性剂蛋白C，在缺氧条件下会减少。具体而言，在缺氧条件下培养8 h后，SpC的原表达会适度降低，在48 h后会完全减弱。高碳酸血症仅在暴露48 h后才降低SpC的表达。在低氧和高碳酸血症的情况下，用TNF-α刺激可部分逆转pSPC的下降。缺氧培养A549细胞会导致细胞逐渐进入细胞周期的G1期，并在暴露后4 h首先观察到凋亡增加，并在24 h达到峰值。相反，高碳酸血症对肺泡上皮细胞增殖或凋亡没有明显影响。结论：总之，我们可以得出结论，缺氧会迅速而严重地影响AECII的功能和生存能力，而高碳酸血症仅在长时间暴露后才对SpC的产生产生抑制作用。

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