Hypoxia enhances transcytosis in intestinal enterocytes

D. Maltseva, M. Shkurnikov, S. Nersisyan, S. Nikulin, A. Kurnosov, M. Raigorodskaya, A. Osipyants, EA Tonevitsky
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Abstract

The integrity of the intestinal epithelial cell lining is crucial for the normal intestinal function. As a rule, intestinal inflammation is associated with additional tissue hypoxia, leading to the loss of epithelial monolayer integrity. However, in the absence of visible damage to the epithelium, there still might be a risk of infection driven by changes in the intracellular transport of bacteria-containing vesicles. The aim of this study was to investigate the effects of hypoxia on transcytosis using a human intestinal enterocyte model. We found that hypoxia enhances transcytosis of the model protein ricin 1.8-fold. The comparative transcriptome and proteome analyses revealed significant changes in the expression of genes involved in intracellular vesicle transport. Specifically, the expression of apoB (the regulator of lipid metabolism) was changed at both protein (6.5-fold) and mRNA (2.1-fold) levels. Further research is needed into the possible mechanism regulating gene expression in intestinal erythrocytes under hypoxic conditions.
缺氧促进肠上皮细胞的胞吞作用
肠道上皮细胞的完整性对肠道的正常功能至关重要。通常,肠道炎症与额外的组织缺氧有关,导致上皮单层完整性的丧失。然而,在上皮未见明显损伤的情况下,仍可能存在由含细菌囊泡细胞内运输变化驱动的感染风险。本研究的目的是利用人肠肠细胞模型研究缺氧对胞吞作用的影响。我们发现缺氧使模型蛋白蓖麻毒素的胞吞作用增强1.8倍。比较转录组和蛋白质组分析显示,参与细胞内囊泡运输的基因表达发生了显著变化。具体来说,载脂蛋白ob(脂质代谢调节剂)的表达在蛋白质(6.5倍)和mRNA(2.1倍)水平上都发生了变化。低氧条件下肠红细胞基因表达调控的可能机制有待进一步研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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