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Mifepristone acts as progesterone antagonist of non-genomic responses but inhibits phytohemagglutinin-induced proliferation in human T cells
Author(s) -
C-H Chien,
JungNien Lai,
ChingFong Liao,
O.Y. Wang,
L.M. Lu,
MeiLing Huang,
W.F. Lee,
MeiChi Shie,
Eileen Jea Chien
Publication year - 2009
Publication title -
human reproduction
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.446
H-Index - 226
eISSN - 1460-2350
pISSN - 0268-1161
DOI - 10.1093/humrep/dep099
Subject(s) - mifepristone , progesterone receptor , endocrinology , medicine , antagonist , intracellular , agonist , receptor , stimulation , biology , cell growth , endogeny , microbiology and biotechnology , pregnancy , biochemistry , genetics , cancer , estrogen receptor , breast cancer
Progesterone is an endogenous immunomodulator that suppresses T cell activation during pregnancy. The stimulation of membrane progesterone receptors (mPRs) would seem to be the cause of rapid non-genomic responses in human peripheral T cells, such as an elevation of intracellular calcium ([Ca(2+)](i)) and decreased intracellular pH (pH(i)). Mifepristone (RU486) produces mixed agonist/antagonist effects on immune cells compared with progesterone. We explored whether RU486 is an antagonist to mPRs and can block rapid non-genomic responses and the induction by phytohemagglutinin (PHA) of cell proliferation.

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