Tumor necrosis factor-alpha (TNF-alpha) inhibits expression of mouse placental lactogen-II through TNF-alpha type-I but not type-II receptor.
The aim of this study was to determine whether TNF-alpha inhibits mPL-II secretion through TNF-RI or TNF-RII, and to investigate the gestational profile of TNF-RI and TNF-RII gene expression. The mouse trophoblast cells from day 12 pregnancy were cultured with or without agonistic polyclonal antibodies directed against the individual TNF-alpha receptors, and mPL-II secretion in the medium was assessed by RIA. Anti-TNF-RI antibody significantly inhibited the mPL-II secretion in a dose- and time-dependent manner, but anti-TNF-RII antibody did not. Moreover, the TNF-RII antibody did not influence the inhibitory effect of the TNF-RI antibody on mPL-II secretion. TNF-RI antibody inhibited the mPL-II gene expression by Northern blot analysis. Amount of the gene expression of TNF-RI in the second half of pregnancy was higher than those in the first half of pregnancy both in vitro and in vivo, although the gene expression of TNF-RII was not detectable by Northern blot analysis using poly(A)+RNA. These results suggest that TNF-RI is a main receptor for TNF-alpha in mouse placenta and that TNF-alpha may have an important role in regulating mPL-II secretion after midpregnancy.
Yamaguchi
M
M
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
Kurachi
H
H
Tadokoro
C
C
Sakata
M
M
Yoshimoto
Y
Y
Masumoto
N
N
Tasaka
K
K
Miyake
A
A
D000818:Animals; D015152:Blotting, Northern; D002478:Cells, Cultured; D005260:Female; D005786:Gene Expression Regulation; D051379:Mice; D010920:Placenta / Q000378:metabolism*; D010928:Placental Lactogen / Q000235:genetics* / Q000378:metabolism; D011247:Pregnancy; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology*
D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D010928:Placental Lactogen