Regulation of the chemokine receptor CXCR4 by hypoxia.
Regulation of the chemokine receptor CXCR4 by hypoxia.
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通过缺氧对趋化因子受体CXCR4的调节。
DOI：
10.1084/jem.20030267
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发表时间：
2003-11-03
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细胞对缺氧的适应（Hyp）需要激活转录程序，这些程序协调参与氧气输送（通过血管生成）和代谢适应（通过糖酵解）的基因的表达。在这里，我们描述了氧的可用性是一个决定性的参数，在设置的趋化反应基质衍生因子1（CXCL 12）。低氧浓度诱导不同细胞类型（单核细胞、单核细胞衍生的巨噬细胞、肿瘤相关巨噬细胞、内皮细胞和癌细胞）中CXCL 12受体CXC受体4（CXCR 4）的高表达，这是由于对其特异性配体的趋化反应性增加所致。Hyp对CXCR 4的诱导依赖于Hyp诱导因子1 α的激活和转录物的稳定。在一个接力的多步导航过程中，Hyp-Hyp-inducible factor 1 α-CXCR 4通路可能调节缺氧组织微环境的进出。
Cell adaptation to hypoxia (Hyp) requires activation of transcriptional programs that coordinate expression of genes involved in oxygen delivery (via angiogenesis) and metabolic adaptation (via glycolysis). Here, we describe that oxygen availability is a determinant parameter in the setting of chemotactic responsiveness to stromal-derived factor 1 (CXCL12). Low oxygen concentration induces high expression of the CXCL12 receptor, CXC receptor 4 (CXCR4), in different cell types (monocytes, monocyte-derived macrophages, tumor-associated macrophages, endothelial cells, and cancer cells), which is paralleled by increased chemotactic responsiveness to its specific ligand. CXCR4 induction by Hyp is dependent on both activation of the Hyp-inducible factor 1 α and transcript stabilization. In a relay multistep navigation process, the Hyp–Hyp-inducible factor 1 α–CXCR4 pathway may regulate trafficking in and out of hypoxic tissue microenvironments.