title: The endocrinology of menstruation--a role for the immune system.
abstract: The human endometrium displays characteristic features, both structural and functional, across the menstrual cycle. It is the sex steroid hormones, oestrogen and progesterone, that drive the endometrium through the different phases of the cycle. Oestrogen and progesterone act sequentially to regulate cellular concentrations of their respective receptors, this interaction initiates gene transcription. Thereafter a cascade of local events prepares the endometrium for implantation, but in the absence of pregnancy, progesterone withdrawal leads to menstruation and cyclic repair. Withdrawal of progesterone from an oestrogen-progesterone primed endometrium is the initiating event for the cascade of molecular and cellular interactions that result in menstruation. Progesterone withdrawal first affects cells with progesterone receptors. Early events in the menstrual process are vasoconstriction and cytokine up-regulation. The activation of lytic mechanisms is a later event and involves cells that may lack progesterone receptors, for example, uterine leucocytes and epithelial cells. Hence progesterone withdrawal results in a local increase of inflammatory mediators and the enzymes responsible for tissue breakdown. The total complex of local factors implicated in normal menstrual and aberrant menstrual bleeding are yet to be fully defined.
authors.affiliation: Centre for Reproductive Biology, The University of Edinburgh, UK. Hilary.Critchley@ed.ac.uk
authors.forename: H O
authors.initials: HO
authors.lastname: Critchley
authors.forename: R W
authors.initials: RW
authors.lastname: Kelly
authors.forename: R M
authors.initials: RM
authors.lastname: Brenner
authors.forename: D T
authors.initials: DT
authors.lastname: Baird
mesh_terms: D000328:Adult; D004717:Endometrium / Q000378:metabolism*; D016228:Endothelial Growth Factors / Q000378:metabolism; D004958:Estradiol / Q000502:physiology*; D005260:Female; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D007107:Immune System / Q000502:physiology*; D018836:Inflammation Mediators / Q000378:metabolism; D008222:Lymphokines / Q000378:metabolism; D020782:Matrix Metalloproteinases / Q000378:metabolism; D008598:Menstruation / Q000502:physiology*; D011374:Progesterone / Q000502:physiology*; D020794:Receptor Protein-Tyrosine Kinases / Q000378:metabolism; D017978:Receptors, Growth Factor / Q000378:metabolism; D040262:Receptors, Vascular Endothelial Growth Factor; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D018836:Inflammation Mediators; D008222:Lymphokines; D017978:Receptors, Growth Factor; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; D011374:Progesterone; D004958:Estradiol; D020794:Receptor Protein-Tyrosine Kinases; D040262:Receptors, Vascular Endothelial Growth Factor; D020782:Matrix Metalloproteinases