z-logo
Premium
GM‐CSF induces expression of gp91 phox and stimulates retinoic acid‐induced p47 phox expression in human myeloblastic leukemia cells
Author(s) -
Shimizu Takahisa,
Kodama Reiko,
Tsunawaki Shohko,
Takeda Ken
Publication year - 2002
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1034/j.1600-0609.2002.01627.x
Subject(s) - retinoic acid , nadph oxidase , microbiology and biotechnology , granulocyte macrophage colony stimulating factor , chemistry , tretinoin , gene expression , acute myeloblastic leukemia , leukemia , biochemistry , cancer research , biology , immunology , reactive oxygen species , gene , in vitro
  All‐ trans retinoic acid (ATRA) combined with granulocyte macrophage colony‐stimulating factor (GM‐CSF) synergistically increases superoxide‐generating activity in human myeloblastic leukemia ML‐1 cells. ATRA is known to increase the expression of some NADPH components; however, little is known about the effect of GM‐CSF on the expression of these components. We examined the expression of NADPH oxidase components in ML‐1 cells treated with ATRA, GM‐CSF, or a combination of ATRA and GM‐CSF. Expression of p47 phox and gp91 phox proteins increased markedly after treatment with both reagents. p47 phox expression was increased by ATRA alone, and the expression was increased synergistically by the combination of ATRA with GM‐CSF. gp91 phox was increased by ATRA or GM‐CSF alone. The expression of p47 phox and gp91 phox mRNA underwent similar changes to those seen in protein level. These results indicate that GM‐CSF induces expression of gp91 phox and enhances ATRA‐induced p47 phox expression. We speculate that the remarkable induction of gp91 phox and p47 phox protein is associated with an increase in superoxide‐generating activity due to the synergistic effect of ATRA plus GM‐CSF.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here