PMID- 2179000
OWN - NLM
STAT- MEDLINE
DCOM- 19900419
LR  - 20190813
IS  - 0303-7207 (Print)
IS  - 0303-7207 (Linking)
VI  - 68
IP  - 2-3
DP  - 1990 Jan 22
TI  - Progesterone modulation of gonadotropin secretion by dispersed rat pituitary 
      cells in culture. II. Intracellular metabolism and progestin receptors.
PG  - 95-103
AB  - Dispersed, estradiol (E2)-treated, rat pituitary cell cultures were used to 
      examine the intracellular processing of progesterone (P) associated with its 
      modulation of gonadotropin-releasing hormone (GnRH)-stimulated luteinizing 
      hormone (LH) secretion. Enhancement and suppression of LH release was only 
      observed with acute and chronic exposures to P or other naturally occurring and 
      synthetic progestins avidly bound by pituitary progestin receptors; such 
      responses were inhibited by cotreatment with the antiprogestin RU486 but not with 
      the antiandrogen flutamide, illustrating the importance of the P + receptor 
      interactions. However, cotreatment with a 100-fold molar excess of the 5 
      alpha-reductase inhibitor 17 beta-N,N-diethyl-carbamoyl-4-methyl-4-aza-5 
      alpha-androstan-3-one (4-MA) had no effect on the expression of P's modulatory 
      actions. Additional studies using different E2 pretreatments revealed that P 
      enhanced LH release when progestin receptor levels were elevated. Moreover, the 
      magnitude and duration of P's influences on LH release increased in cells with 
      higher receptor levels. However, there were several instances in which progestin 
      receptor level and P modulation of LH release did not correlate. In several 
      instances E2-induced progestin receptor levels stabilized at a maximal level 
      whereas P enhancement of LH secretion continued to increase in size and duration. 
      These findings underscore the importance of progestin receptors for P-induced 
      modulation of LH secretion and illustrate that 5 alpha-reduction and further 
      metabolism of P is not obligatory for the expression of these responses. In 
      addition, our data demonstrate that the important cellular mechanisms underlying 
      E2 priming of gonadotroph responsiveness to P entail the induction of progestin 
      receptor levels and other as yet unidentified cellular processes.
FAU - Krey, L C
AU  - Krey LC
AD  - Laboratory of Neuroendocrinology, Rockefeller University, New York, NY 10021.
FAU - Kamel, F
AU  - Kamel F
FAU - MacLusky, N J
AU  - MacLusky NJ
LA  - eng
GR  - HD 10168/HD/NICHD NIH HHS/United States
GR  - HD 19236/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - Ireland
TA  - Mol Cell Endocrinol
JT  - Molecular and cellular endocrinology
JID - 7500844
RN  - 0 (Androgen Antagonists)
RN  - 0 (Azasteroids)
RN  - 0 (Progestins)
RN  - 0 (Receptors, Progesterone)
RN  - 08J2K08A3Y (Dihydrotestosterone)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - 4TI98Z838E (Estradiol)
RN  - 73671-86-0 (17-N,N-diethylcarbamoyl-4-methyl-4-azaandrostane-3-one)
RN  - 9002-67-9 (Luteinizing Hormone)
SB  - IM
MH  - Androgen Antagonists/pharmacology
MH  - Animals
MH  - Azasteroids/pharmacology
MH  - Cells, Cultured
MH  - Dihydrotestosterone/analogs & derivatives/pharmacology
MH  - Estradiol/pharmacology
MH  - Gonadotropin-Releasing Hormone/pharmacology
MH  - Luteinizing Hormone/metabolism
MH  - Pituitary Gland, Anterior/drug effects/*metabolism
MH  - Progesterone/*pharmacology
MH  - Progestins/pharmacology
MH  - Rats
MH  - Receptors, Progesterone/drug effects/*metabolism
EDAT- 1990/01/22 00:00
MHDA- 1990/01/22 00:01
CRDT- 1990/01/22 00:00
PHST- 1990/01/22 00:00 [pubmed]
PHST- 1990/01/22 00:01 [medline]
PHST- 1990/01/22 00:00 [entrez]
AID - 0303-7207(90)90181-7 [pii]
AID - 10.1016/0303-7207(90)90181-7 [doi]
PST - ppublish
SO  - Mol Cell Endocrinol. 1990 Jan 22;68(2-3):95-103. doi: 
      10.1016/0303-7207(90)90181-7.