PMID- 14667999
OWN - NLM
STAT- MEDLINE
DCOM- 20040817
LR  - 20190823
IS  - 0039-128X (Print)
IS  - 0039-128X (Linking)
VI  - 68
IP  - 10-13
DP  - 2003 Nov
TI  - Antiprogestins as a model for progesterone withdrawal.
PG  - 1061-8
AB  - The key physiological function of the endometrium is preparation for 
      implantation; and in the absence of pregnancy, menstruation and repair. The 
      withdrawal of progesterone is the initiating factor for breakdown of the 
      endometrium. The modulation of sex steroid expression and function with 
      pharmacological agents has provided an invaluable tool for studying the 
      functional responses of the endometrium to sex steroids and their withdrawal. By 
      administration of the antiprogestin mifepristone, it is possible to mimic 
      progesterone withdrawal and study local events in early pregnancy decidua that 
      may play a role in the process of early pregnancy failure. Our data indicate that 
      antagonism of progesterone action at the receptor level results in an 
      up-regulation of key local inflammatory mediators, including NF-kappaB, 
      interleukin-8 (IL-8), monocyte chemotactic peptide-1 (MCP-1), cyclooxygenase 2 
      (COX-2) and others in decidua. Bleeding induced by mifepristone in the mid-luteal 
      phase of the cycle is associated with changes in the endometrium similar to those 
      that precede spontaneous menstruation including up-regulation of COX-2 and 
      down-regulation of PGDH. Administration of antagonists of progesterone provide an 
      excellent model to study the mechanisms involved in spontaneous and induced 
      abortion as well as providing information which may help devise strategies for 
      treating breakthrough bleeding associated with hormonal contraception.
FAU - Critchley, Hilary O D
AU  - Critchley HO
AD  - Obstetrics and Gynaecology, Centre for Reproductive Biology, University of 
      Edinburgh, Chancellor's Building, 49 Little France Crescent, Edinburgh EH16 4SB, 
      Scotland, UK. hilary.critchley@ed.ac.uk
FAU - Kelly, Rodney W
AU  - Kelly RW
FAU - Brenner, Robert M
AU  - Brenner RM
FAU - Baird, David T
AU  - Baird DT
LA  - eng
GR  - RR-00163/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PT  - Review
PL  - United States
TA  - Steroids
JT  - Steroids
JID - 0404536
RN  - 0 (Hormone Antagonists)
RN  - 0 (Progestins)
RN  - 320T6RNW1F (Mifepristone)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - EC 2.7.10.1 (Receptors, Vascular Endothelial Growth Factor)
SB  - IM
MH  - Decidua/drug effects
MH  - Embryo Implantation
MH  - Endometrium/drug effects/metabolism
MH  - Female
MH  - Hormone Antagonists/*pharmacology
MH  - Humans
MH  - Luteal Phase
MH  - Menstruation/drug effects
MH  - Mifepristone/pharmacology
MH  - Models, Biological
MH  - Pregnancy
MH  - Progesterone/*metabolism
MH  - Progestins/*antagonists & inhibitors
MH  - Receptors, Vascular Endothelial Growth Factor/metabolism
MH  - Up-Regulation
RF  - 70
EDAT- 2003/12/12 05:00
MHDA- 2004/08/18 05:00
CRDT- 2003/12/12 05:00
PHST- 2003/12/12 05:00 [pubmed]
PHST- 2004/08/18 05:00 [medline]
PHST- 2003/12/12 05:00 [entrez]
AID - S0039128X03001272 [pii]
AID - 10.1016/j.steroids.2003.07.001 [doi]
PST - ppublish
SO  - Steroids. 2003 Nov;68(10-13):1061-8. doi: 10.1016/j.steroids.2003.07.001.