Multiple forms of rat placental lactogen-II (rPL-II): Purification and partial characterization of rPL-II

Kishi, Kurajiro; Hirashiba, Masahiro; Hasegawa, Yasuhiko

doi:10.1016/0143-4004(92)90008-h

Cited by 9 publications

(10 citation statements)

References 34 publications

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“…The 20.5K protein was predominant in amniotic with the same mol wt as the 20.5K was also detected in maternal serum of day 13 pregnant rats, indicating that the largest form (20.5K) of monomeric rPL-II is predominant in amniotic pregnancy. These data also indicate that most of the rPL-II exists as a monomeric form in maternal serum and amniotic fluid during mid pregnancy in contrast to the observation that the dimer or aggregated forms of rPL-II are predominant in maternal serum on day 18 of pregnancy [25]. The physiological roles and biological activities of rPL-II and its variants in amniotic fluid and maternal circulation remain to be determined.…”

Section: Discussioncontrasting

confidence: 39%

“…The proteins electrophoresed on the gel were transferred to PVDF membrane (Clear blot membrane-p, ATTO, Tokyo) for 1 h at 0.27 A. The membrane was incubated with rabbit anti-rPL-II serum and goat anti-rabbit immunoglobulin-alkaline phosphatase conjugate (Bio-Rad), and then developed with the Bio-Rad AP color development reagents described previously [25]. Identical samples were also electrophoresed separately on another gel and stained with silver nitrate [27] for to estimate molecular size.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

1991

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Section: Discussioncontrasting

confidence: 39%

Section: Introductionmentioning

confidence: 99%

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

1991

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“…The lactogenic activity of the plasma samples was estimated by RRA as described previously by Kishi et al (14). All procedures were carried out at room temperature.…”

Section: Estimation Of Lactogenic Activity By Radioreceptor Assay (Rra)mentioning

confidence: 99%

Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats

Kawai

Kishi²

1999

European Journal of Endocrinology

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In rodents, placental lactogen (PL)-I is considered to be the first trigger to enhance pancreatic islet B-cell function, and after its secretion is diminished at mid-pregnancy, PL-II takes over this role. However, little information is available on the regulation of islet B-cell function and proliferation by lactogenic hormones during the last third of pregnancy. This was the focus of the present study using rats in which pregnancy was forcibly prolonged. This rat possesses unique characteristics in that PL-I is re-secreted during the prolonged period of pregnancy and the peak concentrations in maternal circulation are comparable with those observed during mid-pregnancy in normal-pregnancy rats. Pregnancy was prolonged by successive administration of pregnant mare's serum gonadotropin (30 IU/rat, s.c. on day 12) and human chorionic gonadotropin (10 IU/rat, i.v. on day 14). When the insulin secretory responses to 10 mmol/l glucose in islets obtained from normal-pregnancy and prolonged-pregnancy rats were tested, each insulin secretory response correlated well with the values of plasma lactogenic activity throughout the period of pregnancy and lactation. Examination of B-cell proliferation in normal-pregnancy rats showed that 5-bromo-2 0 -deoxyuridine (BrdU) incorporation into dividing B-cells reached a maximum on day 15 and then decreased markedly towards term. No increase in B-cell proliferation was observed on day 19 when plasma lactogenic activity reached the maximum. In prolonged-pregnancy rats, BrdU incorporation also continued to decrease as observed in normal-pregnancy rats after day 15, and then no enhancement in B-cell proliferation was observed even when the plasma lactogenic activity, including re-secreted PL-I, reached maximum. These results suggest that, in the last third of pregnancy, B-cell proliferation is no longer stimulated by lactogenic hormones in contrast to the insulin secretory response which is sustained.

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“…However, it is not clear whether the cAMP analog inhibits rPL-I or rPL-II secretion because the available assay did not discriminate between rPL-I and rPL-II. We recently established an RIA for rPL-II (12,13), and we report here that 8-bromo-cAMP, but not EGF, IL-1 or IL-6, inhibits rPL-II secretion by a rat choriocarcinoma cell line, Rcho-1. Purified mouse EGF (mEGF) was obtained from Collaborative Research (Bedford, MA).…”

mentioning

confidence: 87%

“…Rat PL-II cDNA (14) and mPL-II (15) were kind gifts from Drs ML Duckworth (The University of Manitoba, Manitoba, Canada) and F Talamantes (University of California, Santa Cruz, CA). Rat PL-II and the antiserum for rPL-II were obtained as described previously (12,13 (16) and were used up to 20 passages. They were suspended in a culture medium (NCTC-135 containing 20mmol/l HEPES, 25 mmol/1 NaHC03, 50/xmol/l 2-mercaptoethanol, 1 mmol/1 sodium pyruvate, 100 mg/l penicillin and 105U/1 streptomycin) containing 10% heat-inactivated fetal bovine serum (FBS).…”

mentioning

confidence: 99%

Regulation of rat placental lactogen (rPL)-II secretion: cAMP inhibits rPL-II secretion in vitro

Yamaguchi

Kawai²,

Kishi³

et al. 1995

European Journal of Endocrinology

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We examined whether epidermal growth factor (EGF), interleukin (IL)-1, IL-6 and cAMP analogs, which regulate mouse placental lactogen II secretion, affect rat placental lactogen (rPL)-II secretion using a rat choriocarcinoma cell line, Rcho-1. EGF, IL-1 and IL-6 did not affect rPL-II secretion, but 8-bromo-cAMP and forskolin inhibited rPL-II secretion by the 8th day of culture. The effects were dose dependent and the lowest concentrations of 8-bromo-cAMP and forskolin that significantly inhibited rPL-II secretion were 125 and 5 mumol/l, respectively. Cholera toxin also inhibited rPL-II secretion. The reverse hemolytic plaque assay for rPL-II indicated that the cells releasing rPL-II in the culture were giant cells and that 8-bromo-cAMP decreased the number of rPL-II-releasing cells. Western blot analysis of rPL-II yielded a single band at approximately 24.5 K, and 8-bromo-cAMP treatment significantly reduced the band intensity. Northern blot analysis of rPL-II indicated that 8-bromo-cAMP also reduced rPL-II gene expression. These findings suggest that the increase of intracellular cAMP accumulation results in inhibition of rPL-II secretion by decreasing rPL-II gene expression and inhibiting giant cell differentiation.

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Multiple forms of rat placental lactogen-II (rPL-II): Purification and partial characterization of rPL-II

Cited by 9 publications

References 34 publications

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

Gestational Profiles of Rat Placental Lactogen-II(rPL-ll) and Growth Hormone(GH) im Maternal and Fetal Serum, Amniotic Fluid, and Placental Tissue.

Adaptation of pancreatic islet B-cells during the last third of pregnancy: regulation of B-cell function and proliferation by lactogenic hormones in rats

Regulation of rat placental lactogen (rPL)-II secretion: cAMP inhibits rPL-II secretion in vitro

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