Transferrin gene expression in the mammary gland of the rat. The enhancing effect of 17β-oestradiol on the level of RNA is tissue-specific

1993 ◽  
Vol 11 (2) ◽  
pp. 151-159 ◽  
Author(s):  
R Escalante ◽  
L-M Houdebine ◽  
M Pamblanco
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Fold Increase ◽  
Mammary Glands ◽  
Mammary Tissue ◽  
Specific Response ◽  
Mrna Levels ◽  
Dot Blot ◽  
Pregnant Rats ◽  
Transferrin Gene

ABSTRACT We have investigated the physiological factors which regulate transferrin gene expression in the mammary gland of the rat. Our studies by dot blot analysis have demonstrated that multiple doses of 17β-oestradiol (OE2; 0·5 mg/kg per day for 3 days) elicit a specific 3·5-fold increase in the transferrin mRNA levels in the mammary glands of virgin rats. The hormonal action of OE2 in mammary tissue was specific for the transferrin gene, as judged by hybridization with β-actin cDNA. The accmulation of transferrin mRNA induced by OE2 treatment was similar to the developmentally regulated expression of the gene observed during the reproductive cycle. The steady-state level of mammary transferrin mRNA increased by up to 4·5-fold at day 21 of lactation, when compared with virgin and pregnant rats. Our results show that the pattern of transferrin gene expression is different in mouse and rat mammary glands. The specific response of the transferrin gene to OE2 was not found in the liver or in the uterus. In the uterus alone, OE2 produced a significant increase in the content of nucleic acids and also induced the accumulation of transferrin and β-actin mRNAs. We have detected for the first time an induction of transferrin gene expression in the mammary gland in response to OE2, and these results support the view that the pattern of transferrin gene multimodulated expression is tissue- and species-specific.

Nuclear targeting of stanniocalcin to mammary gland alveolar cells during pregnancy and lactation

2005 ◽  
Vol 289 (4) ◽  
pp. E634-E642 ◽  
Author(s):  
Craig P. Hasilo ◽  
Christopher R. McCudden ◽  
J. Ryan J. Gillespie ◽  
Kathi A. James ◽  
Edward R. Hirvi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Molecular Mass ◽  
Chemical Reduction ◽  
Mammary Tissue ◽  
Nuclear Targeting ◽  
Alveolar Cells ◽  
Hormone Production ◽  
Pregnant Rats ◽  
Pregnancy And Lactation

In most mammalian tissues, the stanniocalcin-1 gene (STC-1) produces a 50-kDa polypeptide hormone known as STC50. Within the ovaries, however, the STC-1 gene generates three higher-molecular-mass variants known as big STC. Big STC is targeted locally to corpus luteal cells to block progesterone release. During pregnancy and lactation, however, ovarian big STC production increases markedly, and the hormone is released into the serum. During lactation, this increase in hormone production is dependent on a suckling stimulus, suggesting that ovarian big STC may have regulatory effects on the lactating mammary gland. In this report, we have addressed this possibility. Our results revealed that virgin mammary tissue contained large numbers of membrane- and mitochondrial-associated STC receptors. However, as pregnancy progressed into lactation, there was a decline in receptor densities on both organelles and a corresponding rise in nuclear receptor density, most of which were on milk-producing, alveolar cells. This was accompanied by nuclear sequestration of the ligand. Sequestered STC resolved as one ∼135-kDa band in the native state and therefore had the appearance of a big STC variant. However, chemical reduction collapsed this one band into six closely spaced, lower-molecular-mass species (28–41 kDa). Mammary gland STC production also underwent a dramatic shift during pregnancy and lactation. High levels of STC gene expression were observed in mammary tissue from virgin and pregnant rats. However, gene expression then fell to nearly undetectable levels during lactation, coinciding with the rise in nuclear targeting. These findings have thus shown that the mammary glands are indeed targeted by STC, even in the virgin state. They have further shown that there are marked changes in this targeting pathway during pregnancy and lactation, accompanied by a switch in ligand source (endogenous to exogenous). They also represent the first example of nuclear targeting by STC.

Gene expression of leptin, leptin receptor, prolactin receptor and whey acidic protein in mammary glands of late-pregnant gilts from two breeds

2004 ◽  
Vol 84 (4) ◽  
pp. 621-629 ◽  
Author(s):  
M. F. Palin ◽  
D. Beaudry ◽  
C. Farmer
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Leptin Receptor ◽  
Prolactin Receptor ◽  
Mammary Glands ◽  
Whey Acidic Protein ◽  
Acidic Protein ◽  
Mrna Levels ◽  
Parenchymal Tissue ◽  
Receptor Mrna

In order to identify genes which are essential for pig mammary gland development, mRNA levels of prolactin receptor (PRL-R), leptin, leptin receptor and whey acidic protein (WAP) were measured in parenchymal tissue of 110-d-pregnant gilts. Thirteen Upton-Meishan (UM) and 14 Large White (LW) pregnant gilts and 5 non-pregnant control gilts (2 LW and 3UM) were used. PRL-R and WAP mRNA levels were higher in pregnant than in non-pregnant gilts (P < 0.05). Leptin mRNA levels were higher in UM than in LW gilts (P < 0.05), but this breed effect was not seen when leptin mRNA levels were corrected for percent fat in parenchyma. Correlations were found between concentrations of IGF-I in plasma and PRL-R (P < 0.01) and WAP (P < 0.05) mRNA levels in UM gilts. Serum prolactin (PRL) was correlated with leptin mRNA levels in the overall (P < 0.05) and LW (P < 0.05) populations of gilts, while estradiol was associated with leptin receptor mRNA in UM gilts (P < 0.05). The mRNA levels of all studied genes were positively correlated with mammary parenchymal and extra parenchymal weights in UM gilts, whereas these variables were only correlated with PRL-R and WAP gene expression in LW gilts. The presence of leptin and leptin receptor mRNA in parenchymal tissue suggests a paracrine role for leptin in mammary tissue of late-pregnant gilts. These results also suggest that the PRL signalling pathway is fully active at the transcriptional level in the mammary gland of gilts at 110 d of pregnancy. Key words: Genetics, pig, mammary glands, Meishan, mRNA

Expression levels of STAT5A and STAT5B in mammary parenchymal tissue from Upton-Meishan and Large White gilts

2002 ◽  
Vol 82 (4) ◽  
pp. 507-518 ◽  
Author(s):  
M. F. Palin ◽  
D. Beaudry ◽  
C. Roberge ◽  
C. Farmer
Keyword(s):  
Mammary Gland ◽  
Mammary Gland Development ◽  
Target Genes ◽  
Mammary Glands ◽  
Mammary Tissue ◽  
Mrna Levels ◽  
Large White ◽  
Parenchymal Tissue ◽  
Tissue Weight ◽  
Gland Development

The implication of STAT5A and STAT5B in mammary gland development and maintenance of lactation is well documented in rodents and humans. However, little is known regarding their roles in mammary gland development during gestation in pigs. We identified and analyzed the complete coding sequences of swine STAT5A and STAT5B and evaluated their mRNA levels in mammary glands of gestating gilts (day 110) in two different breeds, Upton-Meishan and Large White. Sequence analysis revealed a new APASA insertion in the STAT5A amino acid sequence that is in close proximity to residue Tyr 699 and whose phosporylation leads to the activation of target genes’ transcription. STAT5A mRNA levels were higher in Upton-Meishan than in Large White. In both breeds, STAT5B mRNA levels were higher than those of STAT5A , which is contrary to what was found in other mammals. A correlation between circulating IGF-I levels and STAT5B mRNA levels in the mammary gland was noticed in the Upton-Meishan breed only. STAT5B mRNA levels in mammary tissue of Large White gilts were highly correlated with extra-parenchymal tissue weight, parenchymal tissue weight, total parenchymal DNA, RNA and RNA/DNA ratio. In Upton-Meishan gilts, correlations were observed only between extra-parenchymal weight and STAT5A and STAT5B mRNA levels. These results indicate that there are significant differences in mRNA levels of STAT5A and STAT5B in the mammary glands of pregnant gilts when compared to other mammals, and between swine breeds. Key words: Mammary glands, signal transducers, pregnancy, kinases, pig, expression

Calcitonin-like immunoreactivity and calcitonin gene expression in the placenta and in the mammary gland of the rat

1988 ◽  
Vol 119 (3) ◽  
pp. 443-451 ◽  
Author(s):  
V. Jousset ◽  
B. Legendre ◽  
P. Besnard ◽  
N. Segond ◽  
A. Jullienne ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Blot Hybridization ◽  
Cdna Probe ◽  
Mammary Glands ◽  
Rat Tissues ◽  
Dot Blot ◽  
Dot Blot Hybridization ◽  
Base Size ◽  
Rat Mammary Gland

Abstract. Recently, the presence of monomeric CT in plasma and milk was reported by others in a lactating woman surgically thyroidectomized. Similarly, the placenta was thought to be a possible source of CT. Since such findings were based exclusively on immunological arguments, we have investigated the CT gene expression in these rat tissues. CT mRNAs were detected by dot-blot hybridization of total RNAs extracted from rat tissues with a 32P-labelled human CT cDNA probe. Subcellular fractions of each tissue were screened for CT-like immunoreactivity using two different antibodies. With one antibody, extracts of the mammary gland and placenta both produced full displacement of labelled human CT from the antiserum and serial dilutions of the extracts gave displacement curves parallel to that of synthetic human CT, which suggests immunological similarity. However, dilution curves were not parallel for the second antibody, and for both antisera, CT-like immunoreactivity was found in all subsellular fractions from nuclei to cytosols. Immunoprecipitation of translation products from poly (A)+RNAs of placenta showed two major bands around 30 kD. Under stringent conditions, the weak hybridization of placental RNAs seen by dot-blot under less stringent conditions disappeared. Northern analyses of total RNAs from the placenta failed to detect mRNA of 1 k base size like in thyroid glands, but hybridization under weak stringent conditions occurred with larger mRNAs (around 4.4 and 2.4 k bases). Immunoprecipitation of translation products from mRNAs of rat mammary glands showed three major bands around 46, 30 and 20 kD. Dot-blot hybridization of total RNAs extracted from mammary glands was also negative. In conelusion, our results suggest that the CT gene is not expressed in the rat placenta and in rat mammary gland, since CT mRNAs were not detected in either tissues.

Developmental expression of pIgR gene in sheep mammary gland and hormonal regulation

2002 ◽  
Vol 69 (1) ◽  
pp. 13-26 ◽  
Author(s):  
AURORE RINCHEV-ALARNOLD ◽  
LUCETTE BELAIR ◽  
JEAN DJIANE
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Hormonal Regulation ◽  
Mrna Level ◽  
Immunohistochemical Analysis ◽  
Developmental Expression ◽  
Secretory Iga ◽  
Mrna Levels ◽  
Immunoglobulin Receptor ◽  
Pregnancy And Lactation

Secretory IgA found in external secretions are constituted by polymeric IgA (pIgA) bound to the extra-cellular part of the polymeric immunoglobulin receptor (pIgR). The receptor mediates transcytosis of pIgA across epithelial cells. The aim of the present study was to analyse the evolution of pIgR expression in the sheep mammary gland during the development of the mammary gland and to analyse its hormonal regulation. Gene expression of the pIgR was analysed in sheep mammary gland during pregnancy and lactation. By Northern Blot analysis, we observed that low levels of pIgR mRNA are expressed until day 70 of pregnancy. Accumulation of pIgR mRNA started during the third part of pregnancy and intensified 3 d after parturition to reach highest levels during established lactation (day 70). In situ hybridization analysis was used to confirm the increase in pIgR gene expression per mammary epithelial cell. In order to examine the hormonal regulation of the pIgR expression, virgin ewes were hormonally treated. Treatment with oestradiol and progesterone increased pIgR mRNA levels slightly. Subsequent addition of glucocorticoids induced a significant accumulation of pIgR mRNA in the mammary gland of the treated animals. Immunohistochemical analysis was performed to verify that the increase of pIgR mRNA level was associated with enhancement of the pIgR protein in mammary cells. No increase of pIgR mRNA levels were observed if PRL secretion was blocked by bromocryptine injections throughout the hormonal procedure. In conclusion, the present experiments suggest that the enhancement of pIgR levels during lactation result from combined effects of both prolactin and glucocorticoids.

scholarly journals Hormonal regulation of retinoic acid-binding proteins in the mammary gland

1981 ◽  
Vol 200 (3) ◽  
pp. 591-595 ◽  
Author(s):  
R G Mehta ◽  
R C Moon
Keyword(s):  
Retinoic Acid ◽  
Mammary Gland ◽  
Protein Content ◽  
Hormonal Regulation ◽  
Protein Concentration ◽  
Mammary Glands ◽  
Pregnant Rats ◽  
Rab Protein ◽  
Low Concentrations ◽  
Retinoic Acid Binding Proteins

A cytosolic retinoic acid-binding (RAB) protein that sediments specifically as a 2S component on sucrose density gradients was detected in the mammary glands of virgin, pregnant and lactating rats. Mammary cytosol from pregnant rats contained significantly higher concentrations of cytosolic RAB protein than did cytosol from either virgin or lactating rats. The glands of pregnant animals exhibited increased concentration of cytosolic RAB protein during the first 5 days of pregnancy, and a steady decline was observed thereafter. The concentration of cytosolic RAB protein dropped to the value observed during lactation on the day 20 of pregnancy. Moreover, throughout lactation, low concentrations of cytosolic RAB protein were maintained. Daily treatment of virgin and lactating animals with 5 micrograms of oestradiol-17 beta for 1 week increased cytosolic RAB protein to concentrations comparable with those seen in pregnant rats. Progesterone, however, did not affect the mammary cytosolic RAB protein content of virgin rats. These results suggest hormonal involvement in the regulation of cytosolic RAB protein concentration of mammary gland during differentiation.

Uteroplacental insufficiency alters the mammary gland response to lactogenic hormones in vitro

2008 ◽  
Vol 20 (4) ◽  
pp. 460 ◽  
Author(s):  
Rachael O'Dowd ◽  
Mary E. Wlodek ◽  
Kevin R. Nicholas
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Postnatal Growth ◽  
Mammary Development ◽  
Mammary Tissue ◽  
Sham Surgery ◽  
Uterine Vessel ◽  
Lactogenic Hormones ◽  
Vessel Ligation

Adequate mammary development and coordinated actions of lactogenic hormones are essential for the initiation of lactation. Pregnancies compromised by uteroplacental insufficiency impair mammary development and lactation, further slowing postnatal growth. It is not known whether the initiation of lactation or galactopoesis is compromised. Uteroplacental insufficiency induced in rats by bilateral uterine vessel ligation (Restricted) or sham surgery (Control) on Day 18 of gestation preceded collection of mammary tissue on Day 20 of pregnancy. Mammary explants were cultured with combinations of insulin, cortisol and prolactin and analysed for α-lactalbumin and β-casein gene expression. Mammary tissue from late pregnant Restricted rats had elevated α-lactalbumin, but not β-casein, mRNA, which is consistent with premature lactogenesis resulting from an early decline in peripheral maternal progesterone. Explants from Restricted rats were more responsive to hormone stimulation after 3 days in culture, indicating that compromised galactopoesis, not lactogenesis, most likely leads to the reduced growth of suckled pups.

Serum transcriptionally regulates Na(+)-K(+)-ATPase gene expression in vascular smooth muscle cells

1997 ◽  
Vol 273 (3) ◽  
pp. C1088-C1099 ◽  
Author(s):  
J. Nemoto ◽  
S. Muto ◽  
A. Ohtaka ◽  
K. Kawakami ◽  
Y. Asano
Keyword(s):  
Gene Expression ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Atpase Activity ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Fold Increase ◽  
Mrna Levels ◽  
Subunit Protein ◽  
Mrna Induction

The present study was designed to examine the effects of serum on Na(+)-K(+)-ATPase alpha 1- and beta 1-subunit gene expression in cultured vascular smooth muscle cells (VSMC) from rat thoracic aortas. Addition of 10% serum to VSMC for 24 h increased Na(+)-K(+)-ATPase activity 1.5-fold and alpha 1- and beta 1-subunit protein levels 1.9-fold. Serum (10%) caused a 3.5-fold increase in alpha 1-mRNA levels and a 6.7-fold increase in beta 1-mRNA levels, with peak elevations at 12 h. The protein synthesis inhibitor cycloheximide abolished serum-mediated beta 1-mRNA induction but did not affect serum-mediated alpha 1-mRNA induction. Protein kinase C (PKC) inhibitors (staurosporine A or calphostin C) or tyrosine kinase (TK) inhibitors (genistein or herbimycin A) significantly reduced serum-mediated beta 1-mRNA induction but had no effect on serum-mediated alpha 1-mRNA induction. Transfection experiments with the 5'-flanking sequences of the alpha 1- or beta 1-subunit genes linked to the luciferase reporter gene revealed that 10% serum caused 2.8- and 6.5-fold increases in luciferase activity, respectively. Among growth factors, only basic fibroblast growth factor (FGF) enhanced luciferase activities for the alpha 1- and beta 1-subunit genes. We conclude that 1) serum stimulates alpha 1- and beta 1-mRNA expression, alpha 1- and beta 1-subunit protein accumulation, and Na(+)-K(+)-ATPase activity; 2) serum-mediated beta 1-mRNA induction partly requires de novo synthesis of intermediate regulatory proteins and activation of PKC and TK, whereas serum-mediated alpha 1-mRNA induction occurs through PKC- and TK-independent mechanisms; 3) the 5'-flanking regions of the alpha 1- and beta 1-subunit genes are serum responsive; and 4) FGF mimics stimulatory effects of serum on promoter activities for the alpha 1- and beta 1-subunit genes.

scholarly journals Alteration in gene expression of branched-chain keto acid dehydrogenase kinase but not in gene expression of its substrate in the liver of clofibrate-treated rats

1996 ◽  
Vol 317 (2) ◽  
pp. 411-417 ◽  
Author(s):  
Harbhajan S. PAUL ◽  
Wei-Qun LIU ◽  
Siamak A. ADIBI
Keyword(s):  
Gene Expression ◽  
Rat Liver ◽  
Fold Increase ◽  
Branched Chain Amino Acids ◽  
The Other ◽  
Mrna Levels ◽  
Keto Acid ◽  
Protein Mass ◽  
Acid Dehydrogenase ◽  
Branched Chain

We previously showed that the oxidation of branched-chain amino acids is increased in rats treated with clofibrate [Paul and Adibi (1980) J. Clin. Invest. 65, 1285–1293]. Two subsequent studies have reported contradictory results regarding the effect of clofibrate treatment on gene expression of branched-chain keto acid dehydrogenase (BCKDH) in rat liver. Furthermore, there has been no previous study of the effect of clofibrate treatment on gene expression of BCKDH kinase, which regulates the activity of BCKDH by phosphorylation. The purpose of the present study was to investigate the above issues. Clofibrate treatment for 2 weeks resulted in (a) a 3-fold increase in the flux through BCKDH in mitochondria isolated from rat liver, and (b) a modest but significant increase in the activity of BCKDH. However, clofibrate treatment had no significant effect on the mass of E1α, E1β, and E2 subunits of BCKDH or the abundance of mRNAs encoding these subunits. On the other hand, clofibrate treatment significantly reduced the activity, the protein mass and the mRNA levels of BCKDH kinase in the liver. In contrast to the results obtained in liver, clofibrate treatment had no significant effect on any of these parameters of BCKDH kinase in the skeletal muscle. In conclusion, our results show that clofibrate treatment increases the activity of BCKDH in the liver and the mechanism of this effect is the inhibition of gene expression of the BCKDH kinase.

scholarly journals Expression of the antiviral protein Mx in peripheral blood mononuclear cells of pregnant and bred, non-pregnant ewes

2001 ◽  
Vol 170 (2) ◽  
pp. R7-11 ◽  
Author(s):  
SJ Yankey ◽  
BA Hicks ◽  
KG Carnahan ◽  
AM Assiri ◽  
SJ Sinor ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Peripheral Blood Mononuclear Cells ◽  
Peripheral Blood ◽  
Mononuclear Cells ◽  
Fold Increase ◽  
Mrna Levels ◽  
Antiviral Protein ◽  
Peripheral Blood Mononuclear ◽  
Blood Mononuclear Cells

Interferon-tau (IFN tau) acts locally on the endometrium to suppress estrogen and oxytocin receptor expression and block luteolysis in ruminants. Systemic administration of conceptus homogenates or recombinant ovine IFN tau does not block luteolysis or enhance pregnancy rates in sheep or cattle, respectively. However, IFN tau up-regulates expression of the antiviral protein Mx throughout the entire uterine wall during early pregnancy. These studies determined if conceptus-derived IFN tau also up-regulates Mx expression in components of the circulating immune system that migrate through the endometrial wall. In experiment one, peripheral blood mononuclear cells (PBMC) were isolated from ewes at D26 post-artificial insemination (AI) and Mx mRNA levels examined by Northern and slot-blot hybridization. Pregnancy resulted in a two-fold increase in Mx mRNA levels compared to bred, non-pregnant ewes at D26. In experiment two, PBMC were isolated from ewes at AI, and every three days from D9 to D30. Results showed a four-fold increase in Mx mRNA levels in PBMC from pregnant versus bred, non-pregnant ewes at D15. Increased Mx mRNA, which remained elevated through D30, was accompanied by increased levels of Mx protein. These results show that pregnancy recognition signaling rapidly induces Mx gene expression in PBMC, and are the first to suggest that IFN tau activates gene expression in components of the circulating immune system.

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