Regulation of platelet-derived growth factor gene expression in mononuclear phagocytes.
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The mechanism of platelet-derived growth factor (PDGF) gene expression was studied using blood monocytes. Resting monocytes constitutively transcribed both PDGF-A and -B genes. Lipopolysaccharide (LPS) -stimulation markedly increased both PDGF-A and -B gene transcription rates. Consistent with the increased transcription rates, PDGF-A mRNA increased continuously after the stimulation. In contrast, PDGF-B mRNA immediately increased and then decreased after the stimulation. Cycloheximide, a protein synthesis inhibitor, increased the levels of PDGF-A and -B mRNA in resting and LPS-stimulated monocytes without affecting PDGF-A and -B gene transcription rates, suggesting <I>de novo</I> synthesized protein factor (s) are involved in the instability of PDGF mRNA. Polymerase chain reaction revealed that resting monocytes expressed only short PDGF-A mRNA species (exon I-V+VII), but LPS-stimulated monocytes expressed long PDGF-A mRNA species (exon I -VII) as well. Both resting and LPS-stimulated monocytes expressed only one PDGF-B mRNA species (exon I-VII) .<BR>LPS-stimulated monocytes released the increased amount of PDGF, and the release of PDGF was inhibited by cycloheximide, suggesting the released PDGF is derived from <I>de novo</I> synthesized PDGF protein. Together, these observations indicate that PDGF gene expression is regulated at the level of PDGF gene transcription, stability and splicing of PDGF mRA, and synthesis of PDGF protein.
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