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Macrophage responses to hypoxia: relevance to disease mechanisms
Author(s) -
Lewis J. S.,
Lee J. A.,
Underwood J. C. E.,
Harris A. L.,
Lewis C. E.
Publication year - 1999
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.66.6.889
Subject(s) - leukocyte extravasation , biology , hypoxia (environmental) , phagocytosis , extravasation , macrophage , stromal cell , hypoxia inducible factors , microbiology and biotechnology , inflammation , immunology , wound healing , cell type , cell , pathology , cancer research , in vitro , gene , medicine , chemistry , biochemistry , genetics , organic chemistry , oxygen
Macrophages are ubiquitous in the stromal compartment of tissues under normal physiological conditions and the number of these cells increases markedly with the onset and progression of many pathological states. The mechanisms underlying this response are well described in such conditions as wound healing and malignant tumors, where tissue‐specific signals enhance the extravasation of blood monocytes and their subsequent differentiation into macrophages. Recent evidence suggests that macrophages may also be stimulated by microenvironmental factors present in diseased tissues to perform distinct, tissue‐specific activities. One such factor, hypoxia (low oxygen tension), results from insufficient vascular perfusion of a given tissue. Various studies have shown that experimental hypoxia alters the morphology, expression of cell surface markers, viability, phagocytosis, metabolic activity, and release of cytokines by macrophages. Here we review the evidence for these macrophage responses to hypoxia, the involvement of co‐stimuli, and their implications for the role of macrophages in various disease processes. Because the intracellular mechanisms mediating the effects of hypoxia on gene expression in other cell types have been characterized recently, we discuss their possible involvement in the effects of hypoxia on gene expression in macrophages. J. Leukoc. Biol. 66: 889–900; 1999.

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