Transforming growth factor-alpha regulates subpopulation of giant cells which secrete mouse placental lactogen-I (mPL-I) and/or mPL-II at midpregnancy.
The aim of this study was to determine whether transforming growth factor-alpha (TGF-alpha) regulates expression of mouse placental lactogen-I (mPL-I) and mPL-II at midpregnancy in vitro. Treatment of placental cells from day 9 of pregnancy with TGF-alpha resulted in stimulation of mPL-I secretion and inhibition of mPL-II secretion in a time- and dose-dependent manner without changing the amount of newly synthesized trichloroacetic acid precipitable proteins and cell viability. Moreover, TGF-alpha increased the intra-cellular mPL-I concentration and immuno-precipitable newly synthesized mPL-I concentration both in the medium and cells. TGF-alpha increased the number of cells containing only mPL-I and cells containing both mPL-I and mPL-II, but decreased that of the cells containing only mPL-II assessed by double immunocytochemistry. TGF-alpha increased the number of cells releasing only mPL-I but decreased the number of cells releasing only mPL-II, however TGF-alpha did not affect the number of cells releasing both mPL-I and mPL-II assessed by sequential reverse hemolytic plaque assay (RHPA). TGF-alpha decreased the expression of mPL-II mRNA, but did not change the expression of mPL-I mRNA. In situ hybridization for epidermal growth factor receptor (EGF-R) after RHPA for mPL-I indicated that giant cells releasing mPL-I express EGF-R mRNA. These findings suggest that TGF-alpha regulates the subpopulation of giant cells which produces and releases mPL-I and mPL-II and it results in an increase of mPL-I secretion and decrease of mPL-II secretion, and suggests possible post-transcriptional stimulation of mPL-I secretion and transcriptional inhibition of mPL-II secretion by TGF-alpha. Giant cells releasing mPL-I express EGF-R mRNA, suggesting direct regulation of giant cell differentiation by EGF and TGF-alpha at midpregnancy.
Yamaguchi
M
M
Department of Obstetrics and Gynecology, Osaka University Medical School, Japan.
Ogura
K
K
Sakata
M
M
Miyake
A
A
D000818:Animals; D004815:Epidermal Growth Factor / Q000502:physiology; D066246:ErbB Receptors / Q000235:genetics; D005260:Female; D015870:Gene Expression; D015726:Giant Cells / Q000502:physiology*; D017403:In Situ Hybridization; D007700:Kinetics; D051379:Mice; D008813:Mice, Inbred ICR; D010928:Placental Lactogen / Q000235:genetics / Q000378:metabolism*; D011247:Pregnancy; D012333:RNA, Messenger / Q000378:metabolism; D016211:Transforming Growth Factor alpha / Q000494:pharmacology*
D012333:RNA, Messenger; D016211:Transforming Growth Factor alpha; C062303:placental lactogen II; C085699:placental lactogen I, rat; D004815:Epidermal Growth Factor; D010928:Placental Lactogen; D066246:ErbB Receptors