title: Cytokines tumor necrosis factor-α and interferon-γ participate in modulation of the equine corpus luteum as autocrine and paracrine factors.
abstract: Knowledge on the regulation of corpus luteum (CL) function in the mare is scarce. In this study, the presence of cytokines tumor necrosis factor alpha (TNF) and interferon gamma (IFNG), and their receptors (TNFRI, TNFRII and IFNRI), was investigated in equine CL throughout the luteal phase. The effects of TNF and IFNG on secretory function and viability of luteal cells were defined in vitro. Cytokine ligands and receptors were present in steroidogenic and endothelial cells. Protein expression for TNF was greater in mid-phase and regressing CL, while TNFRI was increased in regressing CL and TNFRII did not change. IFNG and IFNRI showed the highest expression in regressing CL. Transcription of mRNA for TNF increased from mid-phase to regressing CL and both TNFRI and TNFRII decreased from early to regressing CL. Transcription of mRNA for IFNG was lower in CL from early phase than in mid or regressing luteal phase, while IFNRI expression was not changed. In the early CL, TNF acted to increase P(4) and PGE(2) but decrease PGF(2α) secretion. In the mid luteal phase, TNF increased PGF(2α) secretion and TNF+IFNG decreased PGE(2) secretion. In the regressing luteal phase, TNF, IFNG and TNF+IFNG decreased P(4) and PGE(2) secretion, but TNF and TNF+IFNG increased PGF(2α) secretion by luteal cells. Cell viability was reduced by TNF+IFNG in regressing CL. These data show the presence of cytokines TNF and IFNG, and their receptors, in the equine CL and indicate their potential involvement in regulation of luteal function.
authors.affiliation: CIISA, Technical University of Lisbon, Portugal.
authors.forename: A
authors.initials: A
authors.lastname: Galvão
authors.forename: D J
authors.initials: DJ
authors.lastname: Skarzynski
authors.forename: A
authors.initials: A
authors.lastname: Szóstek
authors.forename: E
authors.initials: E
authors.lastname: Silva
authors.forename: A
authors.initials: A
authors.lastname: Tramontano
authors.forename: A
authors.initials: A
authors.lastname: Mollo
authors.forename: L
authors.initials: L
authors.lastname: Mateus
authors.forename: G
authors.initials: G
authors.lastname: Ferreira-Dias
mesh_terms: D000818:Animals; D019898:Autocrine Communication; D002478:Cells, Cultured; D003338:Corpus Luteum / Q000276:immunology* / Q000473:pathology; D015237:Dinoprost / Q000235:genetics / Q000378:metabolism; D015232:Dinoprostone / Q000235:genetics / Q000378:metabolism; D005260:Female; D005786:Gene Expression Regulation / Q000276:immunology; D006736:Horses / Q000276:immunology*; D007371:Interferon-gamma / Q000235:genetics / Q000378:metabolism*; D008184:Luteal Cells / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D003341:Luteolysis / Q000235:genetics* / Q000276:immunology; D009842:Oligopeptides / Q000235:genetics / Q000378:metabolism; D019899:Paracrine Communication; D017471:Receptors, Interferon / Q000235:genetics / Q000378:metabolism; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000235:genetics / Q000378:metabolism; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism*
chemical_list: D009842:Oligopeptides; D017471:Receptors, Interferon; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; D014409:Tumor Necrosis Factor-alpha; C560821:peptide P4; D007371:Interferon-gamma; D015237:Dinoprost; D015232:Dinoprostone