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Chemokine Regulation of Hematopoiesis and the Involvement of Pertussis Toxin‐Sensitive G αi Proteins
Author(s) -
Broxmeyer Hal E.,
Youn Byung S.,
Kim Chang,
Hangoc Giao,
Cooper Scott,
Mantel Charlie
Publication year - 2001
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2001.tb03580.x
Subject(s) - pertussis toxin , cxc chemokine receptors , chemokine , chemotaxis , chemokine receptor , microbiology and biotechnology , cxcl2 , biology , ccl7 , haematopoiesis , chemistry , immunology , receptor , g protein , signal transduction , stem cell , inflammation , biochemistry
A bstract : Chemokines have been implicated in regulation of various aspects of hematopoiesis, including negative regulation of the proliferation of immature subsets of myeloid progenitor cells (MPCs), chemotaxis of MPCs, and survival enhancement of MPCs after delayed growth factor addition. Since chemokine receptors are seven‐transmembrane‐spanning G‐protein‐linked receptors and the chemotactic effect in vitro of the CXC chemokine SDF‐1 is pertussis toxin (PT)‐sensitive, implying the involvement of Gα i proteins as mediators of SDF‐1‐induced chemotaxis, we evaluated the effects of PT on other chemokine actions influencing MPCs. While the in vitro survival‐enhancing effects of SDF‐1 on GM‐CSF and steel factor‐dependent mouse bone marrow granulocyte macrophage progenitors (CFU‐GM) were pertussis toxin‐sensitive, the suppressive effects of the CC chemokine MIP‐1α and the CXC chemokine IL‐8 on colony formation by GM‐CSF and steel factor‐sensitive CFU‐GM were insensitive to pertussis toxin. These results suggest that not all chemokine‐mediated effects on MPCs are necessarily mediated through pertussis toxin‐sensitive G αi proteins.