Progesterone action in preparation for decidualization.
An attempt has been made to describe several actions of progesterone related to the preparation of the uterus for decidualization. These actions result from classical ligand-receptor interactions as well as from nonreceptor-mediated changes, that is, those imposed by metabolic inactivation of the steroid. By opposing some of the effects of estrogen, the progestogen alters the utilization of NAD in the endometrium to induce an increase in NADP+ production, elevation of the NADP+/NADPH ratio, and inhibition of the rate of degradation of NAD to NAM and ADP-ribose. These changes are correlated with an inhibition or delay in endometrial DNA synthesis and mitosis, an increased potential for differentiation, and the development of uterine sensitivity to decidual induction. A decidual-inducing stimulus can reverse these progestogen-dependent effects rapidly by limiting the rate of synthesis of NADP+ from NAD. Though one possible mechanism for this reversal may include the inhibition of NAD-kinase by cAMP, there is evidence to suggest that such a direct cause-effect relationship is at present tenuous.
Yochim
J M
JM
D000818:Animals; D003656:Decidua / Q000502:physiology*; D010064:Embryo Implantation; D005260:Female; D009243:NAD / Q000378:metabolism; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D011374:Progesterone / Q000378:metabolism / Q000502:physiology*; D051381:Rats; D011960:Receptors, Estrogen / Q000502:physiology; D011980:Receptors, Progesterone / Q000502:physiology; D014599:Uterus / Q000502:physiology*
D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; D009243:NAD; D011374:Progesterone