Immunolocalization of a gonadotropin-releasing hormone receptor site in murine endometrium that mediates apoptosis.
Circumstantial evidence from a previous study indicated that antibodies generated against a synthetic N-terminal extracellular domain mouse pituitary gonadotropin-releasing hormone (GnRH) receptor peptide acted directly on the murine uterus affecting endometrial regression. Affinity-purified polyclonal sheep antibodies were used to assess tissue-specificity of antibody reactions in diestrous mice. Antibody binding was localized by immunofluorescence staining to anterior pituitary gland and endometrium. Ovary, brain, liver, kidneys, heart, lungs, spleen, gastrointestinal tract, adrenal glands, thymus, thyroid gland, muscle, and adipose were unreactive. Fragmented deoxyribonucleic acid, a marker of programmed cell death/apoptosis, was detected by digoxigenin labeling-immunoperoxidase in endometrial (but not pituitary) glands of animals injected with antipeptide antibodies or native ligand. It appears that luteal phase endometrium of mice expresses a GnRH receptor moiety that is coupled to a cell death (endonuclease) transduction pathway.
Murdoch
W J
WJ
Department of Animal Science, University of Wyoming, Laramie, WY 82071, USA.
D000595:Amino Acid Sequence; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D004717:Endometrium / Q000378:metabolism* / Q000648:ultrastructure; D005260:Female; D051379:Mice; D008969:Molecular Sequence Data; D011966:Receptors, LHRH / Q000276:immunology / Q000378:metabolism*; D012756:Sheep
D011966:Receptors, LHRH