PMID- 8275950
OWN - NLM
STAT- MEDLINE
DCOM- 19940207
LR  - 20111117
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 134
IP  - 1
DP  - 1994 Jan
TI  - Tumor necrosis factor-alpha inhibits the synthesis and release of human decidual 
      prolactin.
PG  - 353-7
AB  - Bone marrow-derived cells are major cellular components of human decidua, with 
      macrophages comprising about 30% of the cells in term tissue. Because cytokines 
      released by bone marrow-derived cells are known to affect hormone release in many 
      tissues, we examined whether cytokines affect the release of PRL from human 
      decidual cells. Exposure of primary decidual cell cultures from term pregnancies 
      to tumor necrosis factor-alpha (TNF alpha), interleukin-1 alpha (IL-1 alpha), 
      IL-1 beta, transforming growth factor-beta (TGF beta), and IL-8 caused 
      dose-dependent inhibition of PRL release. Initial inhibition by each of the 
      cytokines was noted after 24 h of exposure, and maximal inhibition of 33-60% 
      occurred after 3 or 4 days. The maximal inhibitions by TNF alpha, IL-1 alpha, 
      IL-1 beta, TGF beta, and IL-8 were 60%, 55%, 46%, 36%, and 33%, respectively, and 
      the half-maximal effective doses of TNF alpha, IL-1 alpha, IL-1 beta, and TGF 
      beta were 70, 2.8, 0.6, and 40 pM, respectively. The cytokine-induced decrease in 
      decidual PRL release was accompanied by a decrease in PRL synthesis. In contrast 
      to the other cytokines, IL-6 had no effect on basal PRL release. TNF alpha, IL-1 
      alpha, IL-1 beta, and IL-8 also inhibited stimulation of the synthesis and 
      release of PRL and PRL mRNA levels in response to insulin. The effect of the 
      cytokines was not due to inhibition of cell proliferation, because the DNA 
      content of the cells was not affected by cytokine treatment. These results 
      strongly suggest that cytokines released by decidual macrophages and other bone 
      marrow-derived cells may have a paracrine role in the regulation of decidual PRL 
      expression.
FAU - Jikihara, H
AU  - Jikihara H
AD  - Division of Endocrinology, Children's Hospital Medical Center, Cincinnati, Ohio.
FAU - Handwerger, S
AU  - Handwerger S
LA  - eng
GR  - HD-15201/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Insulin)
RN  - 0 (Interleukins)
RN  - 0 (Lymphotoxin-alpha)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 9002-62-4 (Prolactin)
SB  - IM
MH  - Cells, Cultured
MH  - Decidua/cytology/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Female
MH  - Humans
MH  - Insulin/pharmacology
MH  - Interleukins/pharmacology
MH  - Lymphotoxin-alpha/pharmacology
MH  - Prolactin/antagonists & inhibitors/genetics/*metabolism
MH  - RNA, Messenger/drug effects/metabolism
MH  - Time Factors
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
AID - 10.1210/endo.134.1.8275950 [doi]
PST - ppublish
SO  - Endocrinology. 1994 Jan;134(1):353-7. doi: 10.1210/endo.134.1.8275950.