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Epidermal growth factor stimulates macrophage colony‐stimulating factor (M‐CSF) mRNA expression and M‐CSF release in cultured murine stromal cells
Author(s) -
Abboud Sherry L.
Publication year - 1992
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1992.tb04557.x
Subject(s) - stromal cell , epidermal growth factor , macrophage colony stimulating factor , growth factor , haematopoiesis , biology , endocrinology , cytokine , colony stimulating factor , medicine , granulocyte macrophage colony stimulating factor , tumor necrosis factor alpha , microbiology and biotechnology , macrophage , cell culture , immunology , cancer research , stem cell , receptor , in vitro , biochemistry , genetics
Summary Macrophage colony‐stimulating factor (M‐CSF) released by stromal cells of the bone marrow microenvironment plays a crucial role in the growth and proliferation of mononuclear cells. Several peptide mitogens including interleukin‐1, tumour necrosis factor, platelet‐derived growth factor and fibroblast growth factor stimulate the release of M‐CSF and may be important in mediating the haematopoietic response to inflammation. Epidermal growth factor (EGF), released from platelets during aggregation, is mitogenic for a variety of cell types and may cause the release of certain cytokines. In this study we used the TC‐1 murine stromal cells which constitutively secrete M‐CSF as a model to study the regulation of M‐CSF in response to EGF. EGF markedly stimulated the steady state expression of M‐CSF mRNA with a peak effect observed at 3 h. This was associated with the release of M‐CSF protein as determined by radioimmunoassay. EGF also stimulated DNA synthesis in a concentration dependent manner. Although TC‐1 cells express GM‐CSF mRNA, this was not induced by EGF. These findings suggest that EGF is a key regulatory molecule for M‐CSF and may indirectly effect haematopoiesis via the release of M‐CSF from stromal cells.