Disease relevance of Prl3b1

• The rPLII gene has been localized to chromosome 17, using a series of hybrid cell lines derived from mouse hepatoma cells (MWTG3) and adult rat hepatocytes; this is the same chromosome designation as the PRL gene itself and other cloned placental members of this gene family [1].
• The addition of PL II at concentrations of 3-100 microgram/ml enhanced the stimulation of bone resorption by submaximal doses of PTH but had little effect on 45Ca release from control unstimulated cultures [2].
• To explore the roles of lactogens in islet function, we generated a stable line of rat insulinoma (INS-1) cells that express rat placental lactogen II (rPLII) constitutively in culture [3].
• We have investigated the secretory patterns of three placental lactogens (PL-alpha, PL-beta and placental lactogen-II) during normal pregnancy and in two prolonged-pregnancy models [4].
• In this paper we describe experiments which investigate the effects of EGF and TGFalpha on rPLI and rPLII mRNA levels in the rat choriocarcinoma cell line, Rcho [5].

High impact information on Prl3b1

• This protein is processed by dog pancreatic microsomes to a 22,000-dalton form, identical in size to rPLII isolated from pregnant rat serum [6].
• In this paper, we describe cDNA clones for rPLII, which have been isolated from a Day 18 rat placental cDNA library [6].
• Rcho-1 cell cultures showed an increase in PL-I and PL-II mRNA expressions during differentiation and which was not affected by high glucose [7].
• These new data suggest an important role for this enhancing fragment in rPLII placental giant cell expression and are the first to implicate a member of the Ets family in the regulation of this gene family [8].
• We previously identified a 3-kb proximal 5'-flanking region of the rat placental lactogen (rPLII) gene that is important for reporter gene transcription in the rat trophoblast cell line, Rcho, and targets expression to the placentas of transgenic mice [8].

Biological context of Prl3b1

• PL-II gene expression also exhibited a circadian rhythm but the direction of the fluctuation was exactly opposite to that of the Mel(1a) gene, such that at night the junctional zone had the strongest expression, while the labyrinth zone had the weakest [9].
• We previously identified an enhancer element in the 5' flanking region of one family member, rat placental lactogen II (rPLII), which could target reporter gene expression to the placenta in transgenic mice; this enhancer functioned in the Rcho rat trophoblast cell line but not in the rat pituitary GC cell line [10].
• Proteomic identification of AP2 gamma as a rat placental lactogen II trophoblast cell-specific enhancer binding protein [10].
• PL-II mRNA could be detected at Day 10 of gestation [11].
• Growth and maturation of Ins-rPLII cells were compared with that of cells transfected stably with an empty expression plasmid (control) and of INS-1 cells treated with exogenous prolactin [3].

Anatomical context of Prl3b1

• Blastocysts recovered on Day 4 of gestation initially showed no detectable expression of PL-I or PL-II; however, after 2 days of culture PL-I protein expression was detectable [11].
• PL-II, PL-Iv, and the PLPs were all expressed in their appropriate molecular forms and cell types in placentas developing in the absence of fetal influence [12].
• In vitro studies of the stimulation of insulin secretion and B-cell proliferation by rat placental lactogen-II during pregnancy in rats [13].
• 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 [14].
• Rat placental lactogen-II (rPL-II) and growth hormone (rGH) in maternal and fetal serum, amniotic fluid, and placental tissue were measured by a homologous radioimmunoassay during the last half of pregnancy. rPL-II appeared first in maternal circulation and the placental tissue on day 11 of pregnancy [15].

Associations of Prl3b1 with chemical compounds

• In vitro treatment of placental tissue with an melatonin agonist, chloromelatonin, greatly decreased PL-II mRNA levels [9].
• We have previously reported that dopamine (DA) can regulate Pit-1 and PL-II gene expressions [16].
• This unique pair of cysteine residues may be responsible for the extreme tendency of hamster PL-II, compared to other members of the GH-PRL-PL family, to form disulfide-bonded hormone-serum protein complexes [17].
• PL II did not enhance the resorptive response to 1,25-dihydroxyvitamin D, prostaglandin E2, osteoclast-activating factor, or bacterial endotoxin [2].
• Poly-L-lysine (PL II; mol wt, 1000-4000) was added to fetal rat bones cultured in a chemically defined medium (BGJ) containing bovine serum albumin in the presence and absence of parathyroid hormone (PTH) [2].

Other interactions of Prl3b1

• The melatonin agonist, chloromelatonin in culture media also decreased the levels of PL-Iv, PL-II and PLP-C mRNA [16].
• The present study was designed to clarify the cellular localization and expression of leptin receptor(s) [OB-R(s)] mRNA including its splice variants and their correlation with the cells which secrete placental hormone, placental lactogen-II (PL-II), in rat placentae [18].
• Ontogeny of placental lactogen-I and placental lactogen-II expression in the developing rat placenta [11].
• The immunochemical analyses used antipeptide antisera directed to amino acids 56-70 of PL-II and amino acids 152-164 of PLP-A [19].
• Cellular localization of rat placental lactogen II and rat prolactin-like proteins A and B by in situ hybridization [20].

Analytical, diagnostic and therapeutic context of Prl3b1

• PL-I and PL-II mRNA expression were assessed by Northern blot analysis and in situ hybridization [11].
• PL-I and PL-II protein expression were determined by Western blot and immunocytochemical analyses [11].
• Northern and immunoblotting analyses indicated that both PL-II mRNA and protein expression were maximal in the junctional zone on day 13 of gestation and declined as gestation proceeded [19].
• Northern blot analysis revealed that the Rcho-1 tumors expressed both PL-I and PL-II, while the HRP-1 tumors did not express either PL [21].
• In the present study, we found that Pit-1 beta is also synthesized in the rat placenta and we tried to examine the effects of dopamine and estrogen on the regulation of Pit-1 alpha, beta and PL-II genes expression using the reverse transcription-polymerase chain reaction (RT-PCR) and Northern blot hybridization [22].

References