title: Prostaglandin E specifically upregulates the expression of the mannose-receptor on mouse bone marrow-derived macrophages.
abstract: The macrophage mannose receptor (MMR) facilitates the binding and internalization of microorganisms and glycoproteins with terminal mannose residues. The receptor is progressively upregulated as bone marrow precursor cells mature into macrophages and thus may serve as a marker of differentiation. Prostaglandins of the E series (PGE) are known inhibitors of monocyte and macrophage precursor proliferation, an effect often associated with cellular maturation. MMR expression was therefore assessed after exposure of bone marrow macrophage precursor (BMMP) cells to these prostanoids. Receptor expression was determined by ligand binding and via immunoprecipitation of newly synthesized receptor molecules. PGE1 and PGE2 at 10(-9)-10(-6) M upregulated MMR surface expression and biosynthesis four- to sixfold in a dose-dependent manner. BMMPs responsive to prostaglandins were characterized by plastic adherence, F4/80 antigen expression, and nonspecific esterase activity. Prostaglandins accelerated the expression of the MMR in cells by 48-72h, with maximal levels of receptor expression being identical in control or treated cells. Thus, prostaglandins enhanced mannose receptor expression in adherent but not fully differentiated macrophage precursors. This effect is specific for PGE and is mimicked by dibutyrl cyclic AMP. These results indicate that prostaglandins accelerate MMR expression and hence the differentiation of macrophage precursor cells. Cells resident in the bone marrow secrete abundant prostaglandins, suggesting that a paracrine mechanism may exist to regulate MMR expression and function.
authors.affiliation: Division of Gastroenterology, Washington University School of Medicine, St. Louis, Missouri 63110.
authors.forename: S
authors.initials: S
authors.lastname: Schreiber
authors.forename: J S
authors.initials: JS
authors.lastname: Blum
authors.forename: J C
authors.initials: JC
authors.lastname: Chappel
authors.forename: W F
authors.initials: WF
authors.lastname: Stenson
authors.forename: P D
authors.initials: PD
authors.lastname: Stahl
authors.forename: S L
authors.initials: SL
authors.lastname: Teitelbaum
authors.forename: S L
authors.initials: SL
authors.lastname: Perkins
mesh_terms: D000262:Adenylyl Cyclases / Q000502:physiology; D000818:Animals; D001853:Bone Marrow / Q000378:metabolism*; D002453:Cell Cycle / Q000502:physiology; D000242:Cyclic AMP / Q000502:physiology; D005786:Gene Expression Regulation; D066298:In Vitro Techniques; D007700:Kinetics; D037181:Lectins, C-Type; D016173:Macrophage Colony-Stimulating Factor / Q000502:physiology; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D008358:Mannose / Q000378:metabolism*; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D051379:Mice; D008805:Mice, Inbred A; D011458:Prostaglandins E / Q000096:biosynthesis / Q000502:physiology*; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000096:biosynthesis; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic / Q000096:biosynthesis*; D012709:Serum Albumin; D012710:Serum Albumin, Bovine / Q000378:metabolism*; D015854:Up-Regulation
chemical_list: D037181:Lectins, C-Type; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; D011458:Prostaglandins E; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D012709:Serum Albumin; C023840:mannose-bovine serum albumin conjugate; D012710:Serum Albumin, Bovine; D016173:Macrophage Colony-Stimulating Factor; D000242:Cyclic AMP; D016186:Receptor, Macrophage Colony-Stimulating Factor; D000262:Adenylyl Cyclases; D008358:Mannose