Expression and regulation of tumor necrosis factor TNF and TNF-receptor family members in the macaque corpus luteum during the menstrual cycle

Marina C. Peluffo, Kelly A. Young, Jon Hennebold, Richard Stouffer

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    16 Scopus citations

    Abstract

    Members of the tumor necrosis factor (TNF)-receptor (R) family may be involved in the tissue remodeling that occurs in the primate corpus luteum (CL) during development and regression. As a first step towards addressing this issue, studies assessed TNF ligand-R expression and regulation in CL collected from monkeys during the early (ECL, Days 3-5), mid (MCL, Days 7-8), mid-late (MLCL, Days 10-11), late (LCL, Days 14-16), and very late (VLCL, menses) luteal phase of the menstrual cycle. CL were also collected after gonadotropin and/or steroid ablation and replacement (with hLH and the progestin R5020) for 3 days at mid-late luteal phase. TNF-a,-p, FAS ligand (FASL), and TNF-R1 mRNA levels were two- to sixfold greater (P <0.05) at the MLCL or LCL phase as compared to earlier (ECL, MCL). In contrast, TNF-R2 and FAS mRNA levels did not change during the luteal phase. Immunohistochemical staining forTNF-p, TNF-R1, TNF-R2, FAS, and FASL was observed in luteal cells, whereas only TNF-p staining was observed in endothelial cells. Several TNF-R components were influenced by LH and/or steroid ablation; notably, steroid ablation reduced (P<0.05) luteal TNF-a, but not TNF-p, mRNA levels, which was prevented by progestin treatment. In contrast, steroid ablation increased (P<0.05) luteal cell immunostaining for FAS and FASL, which was reduced by progestin treatment. Thus, several members of the TNF R-ligand family are expressed in the primate CL in an LH- and/or progestin-dependent manner. Peak expression in the late luteal phase may signify a role for the TNF-R system in death receptor-mediated apoptosis during luteolysis.

    Original languageEnglish (US)
    Pages (from-to)367-378
    Number of pages12
    JournalMolecular Reproduction and Development
    Volume76
    Issue number4
    DOIs
    Publication statusPublished - Apr 2009

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    ASJC Scopus subject areas

    • Genetics
    • Developmental Biology
    • Cell Biology

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