Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro.

Yamaguchi, Masatoshi; Ógren, L.; Southard, Jonathan N.; Kurachi, Hirohisa; Miyake, Akira; Talamantes, Frank

doi:10.1073/pnas.90.24.11905

Cited by 28 publications

(24 citation statements)

References 42 publications

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“…De novo synthesis of trichloroacetic acid (TCA)-precipitable proteins in the cells and medium was assessed by incubating the cells with 25 jiCi of [ 3 H]leucine between 48 and 72 h of culture as described [18].…”

Section: Protein Synthesismentioning

confidence: 99%

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Endo

Yamaguchi

Farnsworth

et al. 1994

Biology of Reproduction

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The initial objective of this study was to establish a placental cell culture system in which the secretion of mouse growth hormone-releasing factor (mGHRF) could be examined during a several-day period. To determine when during pregnancy placental cells begin to express mGHRF, Northern blot analysis was carried out on total RNA from placentas collected on Days 6, 9, 11, 13, 15, 17, and 18 of pregnancy. Mouse GHRF mRNA could be detected as early as Day 11 of pregnancy. Its steady-state levels increased to maximum values on Days 15-17 and then declined slightly on Day 18. Placentas from Day 12 of pregnancy were selected for cell culture. The basal zone and labyrinth were dispersed in collagenase, and the cells were fractionated on a Percoll gradient. Two bands of cells were selected for further study. Both released significant amounts of immunoreactive mGHRF during a 5-day culture period. Effects of prolonged exposure of the cells to 8-bromo-cAMP and to agents that elevate intracellular cAMP concentration were then examined. Treatment of the cells with 0.5 mM 8-bromo-cAMP resulted in a significant decrease in the mGHRF concentration of the medium by the second day of culture. Mouse GHRF secretion was also inhibited by treatment of the cells with 100 ng/ml cholera toxin or 0.1 mM forskolin. The effect of 8-bromo-cAMP was concentration-dependent, with 0.1 mM being the lowest concentration that was active. 8-Bromo-cAMP treatment also reduced the steady-state level of mGHRF mRNA in the cells.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Protein Synthesismentioning

confidence: 99%

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Endo

Yamaguchi

Farnsworth

et al. 1994

Biology of Reproduction

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“…To visualize proteins bound to PY-20, the blots were incubated with 125I-labeled anti-rabbit IgG (0.5 ,uCi/ml; Proc. NatL Acad Sci USA 92 (1995) 2831 autoradiographs was quantified by densitometry (21). Control blots for mPL-I and phosphotyrosine staining were incubated with nonimmune rabbit serum or mouse IgG, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…EGF and hTGF-a were iodinated with lodo-Gen (22 (21). The DNA content of the cells was determined by the method of Hinegardner (24).…”

Section: Methodsmentioning

confidence: 99%

“…Primary cultures of placental cells were established with tissue collected on day 7 of pregnancy (21). Drug treatments were initiated 2 hr after plating and were carried out in serum-free medium.…”

Section: Methodsmentioning

confidence: 99%

“…Western blot analysis for mPL-I and phosphotyrosine was carried out as described (21). AntimPL-I antiserum and PY-20 were used at dilutions of 1:200 and 1:1000, respectively.…”

Section: Methodsmentioning

confidence: 99%

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Opposite effects of transforming growth factor alpha and epidermal growth factor on mouse placental lactogen I secretion.

Yamaguchi

Ógren

Kurachi

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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This study was undertaken to determine whether transforming growth factor a (TGF-a) regulates the production of mouse placental lactogen I (mPL-I) and mPL-II in a manner that is similar to that of epidermal growth factor (EGF), which was previously shown to stimulate mPL-I secretion and inhibit mPL-II secretion. In contrast to the activity of EGF, human (h) and rat (r) TGF-a (each at 100 ng/ml) inhibited secretion ofmPL-I by placental cells isolated from mice on day 7 of pregnancy. Maximum inhibition of mPL-I secretion occurred on the third day of a 5-day culture period and ranged between 37% and 56% in multiple trials. Incubation of cells with hTGF-a and EGF was not followed by a change in the mPL-I concentration of the medium, suggesting the peptides antagonized each other's effects. hTGF-a and rTGF-a inhibited secretion of mPL-II; maximum inhibition ranged between 62% and 84% in multiple trials. The lowest concentrations of hTGF-a that affected mPL-I and mPL-II secretion were 10 ng/ml and 1 ng/ml, respectively. EGF and hTGF-a bound to the same receptors on placental cells, as assessed by cross-linking, and both peptides stimulated receptor phosphorylation, as assessed by Western blot analysis.There are three types of mPL-containing cells in placental cultures: cells that contain only mPL-I, cells that contain only mPL-II, and cells that contain both mPLs. The percentage of each type of mPL-containing cell in the culture was determined by immunostaining. hTGF-ca affected the differentiation of the subpopulations of PL-containing cells in a manner that differed from that of EGF. The data suggest that TGF-a and EGF do not regulate the production of mPL-I and mPL-II in a similar manner.Transforming growth factor a (TGF-a) and epidermal growth factor (EGF) share 30-40% amino acid sequence homology and are believed to act by binding to a common receptor designated the EGF receptor (1, 2). As expected from their binding to a common receptor, effects of EGF and TGF-a have generally been similar, although qualitative and quantitative differences in the responses induced by the peptides have been observed (3-10). We recently examined effects of EGF on the secretion of mouse placental lactogen I (mPL-I) and mPL-II (11), which are prolactin-like hormones produced by trophoblast giant cells (12). mPL-I is present at high concentration in maternal blood on days 9 and 10 of pregnancy (13). mPL-II appears in maternal blood on day 9 of pregnancy and is present at relatively high concentration during the last week of pregnancy (term = 19 days) (14). EGF stimulated the secretion of mPL-I by mouse placental cells from days 7 and 9 of pregnancy and inhibited secretion of mPL-II by cells from days 7, 9, and 12. In addition, the sensitivity of mPL-II-producing cells to EGF declined between days 7 and 12 of pregnancy. These data suggested that EGF may play a role in the shift in placental PL production from mPL-I to mPL-II that occurs at midpregnancy. Effects of TGF-a in this system were not examined. Since TGF-a mRNA and/or...

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Diesel exhaust affects immunological action in the placentas of mice

et al. 2005

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We investigated the effect of diesel exhaust (DE) on pregnancy and fetal development in mice at day 14 postcoitum (pc) with a special focus on the placenta. The number of absorbed fetuses increased in groups exposed to DE, and congestion was observed in histological sections of placentas. During placental absorption expression of CYP1A1 mRNA decreased to undetectable levels, whereas expression of TNF alpha mRNA increased approximately twofold over that of the control. Levels of CYP1A1 mRNA in normal placentas from DE-exposed mice were unchanged. mRNA levels of inflammatory cytokines IL-2, IL-5, IL-12 alpha, IL-12 beta, and GM-CSF increased in placentas exposed to DE (0.3 and 3.0 mg diesel exhaust particles (DEP)/m3). Expression of IL-5 mRNA was markedly increased in DE-exposed placentas, although levels were barely detectable in control placentas. IL-6 mRNA expression was increased approximately 10-fold in placentas exposed to DE (3.0 mg DEP/m3). It has been reported that expression of mRNA encoding proteins involved in immune function in the placenta is increased during fetal absorption in mice. In the present study, expression of such mRNA by the placenta was increased by DE exposure. Because it is believed that expression of mRNA in the placenta also affects fetal development, DE may promote fetal absorption. These findings suggest that in mice exposure to DE affects fetal absorption and placental function by modifying expression of immune-related genes during early gestation and expression of endocrine-related genes during late gestation.

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Interleukin 6 inhibits mouse placental lactogen II but not mouse placental lactogen I secretion in vitro.

Cited by 28 publications

References 42 publications

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Mouse Placental Cells Secrete Immunoreactive Growth Hormone-Releasing Factor1

Opposite effects of transforming growth factor alpha and epidermal growth factor on mouse placental lactogen I secretion.

Diesel exhaust affects immunological action in the placentas of mice

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