Rat Decidual Prolactin. IDENTIFICATION, MOLECULAR CLONING, AND CHARACTERIZATION (original) (raw)
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Decidual prolactin-related protein. Identification, molecular cloning, and characterization
The Journal of biological chemistry, 1993
In this report, we describe the isolation, molecular cloning, and characterization of a new member of the prolactin (PRL)-growth hormone (GH) family expressed in rat decidual tissue. A 29-kDa protein was isolated from medium conditioned by decidual explants. The protein possessed an affinity for concanavalin A and cross-reactivity with antibodies to two rat placental proteins, PRL-like protein-B (PLP-B) and PLP-C and with antibodies to human PRL. NH2-terminal sequencing of the isolated decidual protein indicated that it shared significant sequence identity with the NH2 terminus of PLP-C. The decidual protein was termed decidual prolactin-related protein (dPRP). A PLP-C cDNA was used to identify dPRP cDNAs from a rat decidual cDNA library. Nucleotide sequence analyses of the dPRP cDNAs predicted a mature protein of 239 amino acids, including a 28-amino acid signal sequence. The predicted dPRP amino acid sequence contains two putative N-linked glycosylation sites and 6 cysteine residu...
Decidual Prolactin Silences the Expression of Genes Detrimental to Pregnancy
Endocrinology, 2007
Although the main role of prolactin (PRL) in pregnant rodents is to sustain progesterone production by the corpus luteum, progesterone treatment of PRL or PRL receptor (PRL-R) null mice is unable to prevent fetal loss. We have previously shown that the rat decidua is a site of PRL production and action. In this report, we examined the hypothesis, using PRL null mice and rat decidual cell culture, that the absence of this hormone leads to the expression in the decidua of genes detrimental to pregnancy. The results show that decidual growth is normal in PRL null mice treated with PRL, progesterone, or their combination. However, the decidua of mice treated with progesterone starts expressing IL-6 and 20␣-hydroxysteroid dehydrogenase (20␣-HSD), two proteins absent from the decidua of wild-type mice and involved, respectively, in inflammation and progesterone catabolism. The expression of both IL-6 and 20␣-HSD is prevented by PRL treatment. Our results further
Expression of prolactin-releasing peptide and its receptor in the human decidua
Molecular Human Reproduction, 2002
have been shown to regulate decidual PRL release, but a specific PRL-releasing substance remains to be characterized. Prolactin-releasing peptide (PrRP) is a peptide isolated from the brain and distinguished by its potent and specific stimulation of PRL release by cultured pituitary cells. Here, we demonstrate that human decidua expresses immunoreactive PrRP as well as the mRNAs encoding PrRP and its receptor. First trimester deciduas were obtained from women undergoing elective termination of pregnancy. Tissue specimens were stained by immunohistochemistry using a rabbit anti-human PrRP-31 antibody, and PrRP was localized in both epithelial cells of the decidual glands and in stromal cells, with diffuse distribution and no special relation with the neighbourhood of blood vessels. In primary cultures of decidual stromal cells, PrRP and PrRP receptor gene expression were detected using RT-PCR, and the identity of the PCR products was further confirmed by restriction enzyme digestion. The effect of PrRP on decidual PRL release was also evaluated, and there was a significant increase in PRL production (135 ⍨ 4% of control levels, P < 0.05) after incubation of decidual stromal cells with synthetic PrRP. The expression of PrRP and PrRP receptor in human decidual cells and the ability of PrRP to induce PRL secretion by cultured decidual cells suggests that this peptide may be a novel local modulator of decidual PRL release.
Hormonal Regulation of Prolactin Cell Development in the Fetal Pituitary Gland of the Mouse
Endocrinology, 2009
The developmental process of prolactin (PRL) cells in the fetal pituitary gland was studied in mice. Although PRL cells were hardly detectable in the pituitary gland of intact fetuses, a treatment with 17-estradiol (E 2 ) in vitro induced a number of PRL cells that varied drastically in number depending on the stage of gestation with a peak at embryonic d 15. This effect was specific to E 2, with epidermal growth factor, insulin, and forskolin failing to induce PRL cells. Although both estrogen receptor (ER)␣ and ER were expressed in the fetal pituitary gland, the results from ER knockout models showed that only ER␣ mediates E 2 action on PRL cells. A few PRL cells were observed in ER␣-deficient mice as well as in their control littermates, suggesting that estrogen is not required for the phenotype determination of PRL cells. Unexpectedly, the effect of E 2 on the induction of PRL cells in vitro was diminished after embryonic d 15. Present results suggest that the exposure of fetal PRL cells to glucocorticoids (GCs) results in a reduction of sensitivity to E 2 . The mechanism underlying the down-regulation of estrogen sensitivity by GCs was found not to be down-regulation of ER levels, induction of annexin 1, a GC-inducible inhibitor of PRL secretion, or a decrease in the number of PRL precursors by apoptosis. The effect of GCs appeared within 2 h and did not require a de novo protein synthesis. GCs are considered to be involved in the mechanisms of silencing pituitary PRL in gestation possibly through a novel mechanism.
Endocrinology, 2000
Estradiol is known to play an important role in the growth and differentiation of rat uterine stromal cells into decidual cells. In particular, this hormone with progesterone is necessary for blastocyst implantation and subsequent decidualization in the rat. Although binding experiments have demonstrated the presence of estrogenbinding sites, no evidence exists as to whether the rat decidua expresses both isoforms of the estrogen receptor (ER), ␣ and . In this investigation, we analyzed the expression of decidual ER␣ and ER, studied their regulation by PRL and steroid hormones and examined the ability of decidual ER to transduce the estradiol signal to the progesterone receptor. Immunocytochemistry, RT-PCR, and Northern blot analysis showed that both ER species are coexpressed in the decidua during pseudopregnancy. Interestingly, these genes were preferentially found in a cell population localized in the antimesometrial site of the uterus where blastocyst implantation takes place. Using decidual cells in primary culture obtained from pseudopregnant rats and a decidua-derived cell line (GG-AD), we show a differential regulation of ER␣ and ER by PRL and ovarian steroid hor-
Biochemical and Biophysical Research Communications, 1980
A new form of prolactin which has a cleavage in its large disulphide loop and is synthesised and secreted by rat pituitary glands radioactively labelled in vitro has been detected on sodium dodecyl sulphate polyacrylamide gel analysis and identified by tryptic fingerprinting; this form of prolactin was also found in fresh pituitary glands. The molecule is a 2-chain structure; the 2 component polypeptide chains are separable into an N-terminal 16,000 dalton and a C-terminal 8,000 dalton fragment by the reduction of the intervening disulphide bridge. The cleaved prolactin is a post-translationally modified form of the hormone whose production is regulated by physiological and pharmacological stimuli. ergic inhibitory control of the hypothalamus; and suggested that it could be expected to be synthesised and secreted by the pituitary gland in vitro.
Endocrinology, 2000
Estradiol is known to play an important role in the growth and differentiation of rat uterine stromal cells into decidual cells. In particular, this hormone with progesterone is necessary for blastocyst implantation and subsequent decidualization in the rat. Although binding experiments have demonstrated the presence of estrogenbinding sites, no evidence exists as to whether the rat decidua expresses both isoforms of the estrogen receptor (ER), ␣ and . In this investigation, we analyzed the expression of decidual ER␣ and ER, studied their regulation by PRL and steroid hormones and examined the ability of decidual ER to transduce the estradiol signal to the progesterone receptor. Immunocytochemistry, RT-PCR, and Northern blot analysis showed that both ER species are coexpressed in the decidua during pseudopregnancy. Interestingly, these genes were preferentially found in a cell population localized in the antimesometrial site of the uterus where blastocyst implantation takes place. Using decidual cells in primary culture obtained from pseudopregnant rats and a decidua-derived cell line (GG-AD), we show a differential regulation of ER␣ and ER by PRL and ovarian steroid hormones. Whereas PRL, estradiol, and progesterone all increased ER messenger RNA (mRNA) expression in a dose-dependent manner, only PRL up-regulated the mRNA levels of ER␣. Estradiol had no effect on ER␣ expression, whereas progesterone markedly decreased its mRNA levels. Interestingly, progesterone, which up-regulates the ability of PRL to signal to a PRL-regulated gene in mammary-gland derived cells, prevented PRL stimulation of decidual ER␣ and had no synergistic effect on ER expression. The use of GG-AD cells, which express only ER, allowed us to demonstrate that this receptor subtype is functional and transduces estradiol signal to the progesterone receptor. In summary, the results of this investigation have revealed that ER is expressed in addition to ER␣ in the rat decidua, and that the expression of both ERs are cell specific and differentially regulated by PRL and steroids. One salient finding of this investigation is that progesterone down-regulates ER␣, but concomitantly increases the expression of a functional ER that mediates estradiol up-regulation of the decidual progesterone receptor.
Identification of target genes for a prolactin family paralog in mouse decidua
Reproduction (Cambridge, England), 2015
Prolactin family 8, subfamily a, member 2 (PRL8A2; also called decidual prolactin-related protein; dPRP) is a member of the expanded prolactin family. PRL8A2 is expressed in the uterine decidua and contributes to pregnancy-dependent adaptations to hypoxia. The purpose of this study was to identify gene targets for PRL8A2 action within the uteroplacental compartment. Affymetrix DNA microarray analysis was performed for RNA samples from WT and Prl8a2 null tissues. Validation of the DNA microarray was performed using quantitative RT-PCR. Nine genes were confirmed with decreased expression in Prl8a2 null tissues (e.g., Klk7, Rimklb, Arhgef6, Calm4, Sprr2h, Prl4a1, Ccl27, Lipg, and Htra3). These include potential decidual, endothelial and trophoblast cell targets positively regulated by PRL8A2. A significant upregulation of Derl3, Herpud1, Creld2, Hsp90b1, Ddit3 and Hspa5 was identified in Prl8a2 null tissues, reflecting an increased endoplasmic reticulum (ER) stress response. ER stress ...
Immunohistochemical Study of Postnatal Development of Prolactin-Producing Cells in C57BL Mice
Acta Histochemica et Cytochemica, 1985
Sexual dimorphic changes in postnatal development of prolactin (PRL)producing cells in the anterior pituitary gland in C57BL mice were immunohistochemically investigated. When examined at birth, PRL cells were already present in both male and female mice. With advancement of age, PRL cells increased in number. The shape of PRL cells at birth was oval, but on day 7 irregular-shaped PRL cells appeared. The shape of immunoreactive secretory granules in PRL cells were spherical at birth and also at day 7. However, on day 14 polymorphic PRL granules began to appear in type III PRL cells in both male and female mice. The ratios among type I, II, and III PRL cells and also the total number of all types of PRL cells were not different between male and female mice until 4 weeks of age. Meanwhile, type II PRL cells were predominant in both sexes. From 5 weeks of age, type III PRL cells began to increase in number in female mice only, thus sexual dimorphism in PRL cell types became noticeable during pubertal changes. The present results suggest that postnatal morphological, particularly sexual dimorphic, changes observed in secretory granules as well as cell shapes of PRL cells are mainly due to the reflection of endocrine functions in pubertal female mice.