title: Action of prolactin, IFN-gamma, TNF-alpha and LPS on heme oxygenase-1 expression and VEGF release in human monocytes/macrophages.
abstract: The pituitary hormone prolactin (PRL) has recently been regarded as a local regulator of macrophage responses. Our goal in this study was to investigate the regulatory interaction between PRL, interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha) and lipopolysaccharide (LPS) in the heme oxygenase-1 (HO-1) expression and the vascular endothelial growth factor (VEGF) production in human monocytes/macrophages (HMMs). In vitro treatment of HMMs with PRL, IFN-gamma, TNF-alpha and LPS was found to increase both HO-1 expression and protein synthesis in a time-dependent manner. HMMs treated with PRL, IFN-gamma, TNF-alpha and LPS also showed an enhanced release of VEGF. Moreover, co-stimulation of PRL with LPS caused activation of HMMs functions, enhancement of HO-1 expression and induction of VEGF release, whereas addition of PRL inhibited up-regulation of HO-1 or VEGF induced by IFN-gamma or TNF-alpha. Our results demonstrate that PRL, IFN-gamma, TNF-alpha and LPS modulate the expression of angiogenic factors providing additional information about the regulatory mechanism, which controls the angiogenic function of macrophages.
authors.affiliation: Department of Biomedical Sciences, University of Catania, Via E. De Amicis, 24, 95039 Trecastagni-Catania, Italy.
authors.forename: L
authors.initials: L
authors.lastname: Malaguarnera
authors.forename: R
authors.initials: R
authors.lastname: Imbesi
authors.forename: M
authors.initials: M
authors.lastname: Di Rosa
authors.forename: A
authors.initials: A
authors.lastname: Scuto
authors.forename: P
authors.initials: P
authors.lastname: Castrogiovanni
authors.forename: A
authors.initials: A
authors.lastname: Messina
authors.forename: S
authors.initials: S
authors.lastname: Sanfilippo
mesh_terms: D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D051547:Heme Oxygenase-1; D006801:Humans; D007155:Immunologic Factors / Q000494:pharmacology*; D007371:Interferon-gamma / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D008565:Membrane Proteins; D009000:Monocytes / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D011388:Prolactin / Q000494:pharmacology; D013481:Superoxides / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*
chemical_list: D007155:Immunologic Factors; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; D013481:Superoxides; D007371:Interferon-gamma; D011388:Prolactin; C496541:HMOX1 protein, human; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1