首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Granulocyte-macrophage and macrophage colony-stimulating factors differentially regulate alpha v integrin expression on cultured human macrophages.
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Granulocyte-macrophage and macrophage colony-stimulating factors differentially regulate alpha v integrin expression on cultured human macrophages.

机译:粒细胞巨噬细胞和巨噬细胞集落刺激因子差异性调节培养的人类巨噬细胞上的αv整合素表达。

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摘要

The colony-stimulating factors (CSFs) greatly influence mature macrophage function in vitro: macrophage (M)-CSF induces maturation of monocytes and enhances differentiated cell function; granulocyte-macrophage (GM)-CSF stimulates a variety of antimicrobial functions. In vivo M-CSF is thought to promote differentiation, and GM-CSF is thought to potentiate the inflammatory response. One mechanism by which these differential effects may be achieved is through the receptor-mediated interaction of macrophages with their extracellular matrix. Here we show that M-CSF induces specifically the expression of the alpha v beta 5 integrin receptor, whereas GM-CSF rapidly induces mRNA and surface expression of the alpha v beta 3 integrin. The M-CSF-treated cells acquire a flattened epitheloid phenotype, and on vitronectin the alpha v beta 5 is located in adhesion plaques. These cells do not bind collagen or laminin. In contrast, cells treated with GM-CSF adopt an elongated phenotype on a number of substrates, including collagen and laminin, and express alpha v beta 3 at the leading edge of cells on vitronectin. These results suggest that a primary means by which the CSFs exert their individual effects on mature cells may be through regulating integrin expression.
机译:集落刺激因子(CSFs)在体外极大地影响成熟的巨噬细胞功能:巨噬细胞(M)-CSF诱导单核细胞成熟并增强分化的细胞功能。粒细胞巨噬细胞(GM)-CSF刺激多种抗菌功能。体内M-CSF被认为促进分化,而GM-CSF被认为可增强炎症反应。可以实现这些差异作用的一种机制是通过巨噬细胞与其细胞外基质的受体介导的相互作用。在这里,我们显示M-CSF特异性诱导αv beta 5整合素受体的表达,而GM-CSF快速诱导αv beta 3整合素的mRNA和表面表达。经M-CSF处理的细胞具有扁平的上皮表型,玻连蛋白上的alpha v beta 5位于粘附斑块中。这些细胞不结合胶原蛋白或层粘连蛋白。相反,用GM-CSF处理的细胞在包括胶原蛋白和层粘连蛋白在内的许多底物上采用延长的表型,并在玻连蛋白上的细胞前沿表达αv beta 3。这些结果表明,CSF对成熟细胞发挥其各自作用的主要手段可能是调节整联蛋白的表达。

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