Year-end Sale % OFF 
Abstract
AbstractWe recently showed that mRNA levels coding the high-affinity Fcγ receptor for IgG (FcγR-I, CD64) and two of the components of the phagocytic superoxide anion-generating system—the heavy-chain subunit of cytochrome b558 (gp91-phox) and the 47-Kd cytosolic factor (p47-phox)—are modulated by interferon gamma (IFN-γ). In this study, we examined whether dexamethasone (DEX) affects gp91-phox and p47-phox mRNA expression of human polymorphonuclear leukocytes (PMN), treated or not with IFN-γ. We also investigated whether staurosporine, a general inhibitor of protein kinases, influences gp91-phox, p47-phox, and FcγR-I gene expression in PMN treated with or without IFN-γ. We found that (1) gp91-phox mRNA steady-state levels, expressed in control or IFN-γ-treated PMN, were significantly inhibited, in a dose-dependent fashion, by both DEX and staurosporine; (2) p47-phox mRNA steady-state levels, expressed in control or IFN-γ-treated PMN, were not influenced by DEX, but were markedly depressed by staurosporine; (3) no changes of spectrophotometric cytochrome b558 were found in PMN treated for up to 20 hours with the inhibitors, regardless of the presence of IFN-γ; (4) both DEX and staurosporine dose-dependently inhibited IFN-γ-induced FcγR-I mRNA and protein expression; and (5) stability of gp91-phox and FcγR-I messages in IFN-γ-treated PMN was not altered by the presence of DEX. Our results demonstrate that gp91-phox, p47-phox, and FcγR-I gene expression of PMN is governed by specific and independent biochemical pathways. Moreover, IFN-γ activates different signal transduction pathways to modulate mRNA expression of gp91-phox, p47-phox, and FcγR-I. © 1992 by The American Society of Hematology. 0006-4971/92/7903-0021$3.00/0
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
