scholarly journals 282.Differential expression of the relaxin receptor (LGR7) in the mammary apparatus of the lactating tammar wallaby (Macropus eugenii)

2004 ◽  
Vol 16 (9) ◽  
pp. 282
Author(s):  
J. Gwyther ◽  
H. M. Gehring ◽  
L. J. Parry
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Peptide Hormone ◽  
Tammar Wallaby ◽  
Mammary Glands ◽  
Taqman Probe ◽  
Amino Acid Homology ◽  
Different Ages ◽  
Thermal Cycler ◽  
Relaxin Receptor

Growth and development of the mammary apparatus (nipple and mammary gland) are important aspects of lactation. Macropodid marsupials can suckle young of two different ages simultaneously, a phenomenon known as asynchronous lactation. As a result, the type of milk produced and the structure of the two mammary glands supporting young of different ages vary considerably. A role for the peptide hormone relaxin in lactation has been demonstrated in relaxin receptor (LGR7)-deficient mice, which fail to deliver milk to their offspring due to impaired nipple development (1). This study investigated the distribution of LGR7 in the different mammary glands and nipples during asynchronous lactation in the tammar wallaby. The specific aim was to determine if the age of the pouch young influences LGR7 gene expression. Tissues were collected from the mammary apparatus sustaining the neonate and an older pouch young in the same mother, between Days 0 and 21 of lactation (n = 5/stage). A partial sequence (250-bp) of the tammar LGR7 was first obtained from a region close to the N-terminus of the soluble ectodomain, with 82% amino acid homology compared to the human LGR7 sequence. LGR7 gene expression was then measured by quantitative-PCR, using a TaqMan probe in the Opticon 2 thermal cycler (MJ Research, GeneWorks). Expression of LGR7 was upregulated in both the nipple and mammary gland supporting the neonate between 5 and 11 days after birth. There was no difference in LGR7 expression between these two tissues. However, LGR7 mRNA concentrations were significantly (P < 0.05: paired t-test) higher in the mammary apparatus supporting the neonate compared with that of the older young. These data suggest that a local stimulus, such as the continuous sucking by the neonate, may influence LGR7 expression in the mammary apparatus. (1) Krajnc-Franken et al. (2004) Mol. Cell. Biol. 24, 687–696.

Gene expression in the mammary gland of the tammar wallaby during the lactation cycle reveals conserved mechanisms regulating mammalian lactation

2016 ◽  
Vol 28 (9) ◽  
pp. 1241 ◽  
Author(s):  
C. J. Vander Jagt ◽  
J. C. Whitley ◽  
B. G. Cocks ◽  
M. E. Goddard
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Milk Protein ◽  
Mammary Epithelial Cells ◽  
Tammar Wallaby ◽  
Mammary Epithelial ◽  
Molecular Networks ◽  
Milk Protein Gene ◽  
Milk Protein Gene Expression ◽  
Lactation Cycle

The tammar wallaby (Macropus eugenii), an Australian marsupial, has evolved a different lactation strategy compared with eutherian mammals, making it a valuable comparative model for lactation studies. The tammar mammary gland was investigated for changes in gene expression during key stages of the lactation cycle using microarrays. Differentially regulated genes were identified, annotated and subsequent gene ontologies, pathways and molecular networks analysed. Major milk-protein gene expression changes during lactation were in accord with changes in milk-protein secretion. However, other gene expression changes included changes in genes affecting mRNA stability, hormone and cytokine signalling and genes for transport and metabolism of amino acids and lipids. Some genes with large changes in expression have poorly known roles in lactation. For instance, SIM2 was upregulated at lactation initiation and may inhibit proliferation and involution of mammary epithelial cells, while FUT8 was upregulated in Phase 3 of lactation and may support the large increase in milk volume that occurs at this point in the lactation cycle. This pattern of regulation has not previously been reported and suggests that these genes may play a crucial regulatory role in marsupial milk production and are likely to play a related role in other mammals.

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

207. Effect of TGFB1 on mammary gland development is dependent on cellular source of gene expression

2008 ◽  
Vol 20 (9) ◽  
pp. 7
Author(s):  
W. V. Ingman ◽  
SA Robertson
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Mammary Glands ◽  
Comparable Amount ◽  
Mammary Gland Tissue ◽  
Terminal End Buds ◽  
Cellular Source ◽  
Mammary Gland Morphogenesis ◽  
Gland Morphogenesis ◽  
The Impact

The cytokine TGFB1 is implicated in development of the mammary gland through regulation of epithelial cell proliferation and differentiation during puberty and pregnancy. We have compared mammary gland morphogenesis in virgin Tgfb1+/+, Tgfb1+/− and Tgfb1−/− mice, and transplanted Tgfb1+/+ and Tgfb1−/− epithelium to determine the impact of TGFB1 deficiency on development. When mammary gland tissue was evaluated respective to timing of puberty, invasion through the mammary fat pad of the ductal epithelium progressed similarly irrespective of genotype, albeit fewer terminal end buds were observed in mammary glands from Tgfb1−/− mice. The terminal end buds appeared morphologically normal, and a comparable amount of epithelial proliferation was evident. However, when transplanted into wildtype recipients, Tgfb1−/− epithelium showed accelerated invasion compared with Tgfb1+/+ epithelium. This suggests that the normal rate of ductal extension in Tgfb1−/− null mutant mice is the net result of impaired endocrine or paracrine support acting to limit the consequences of unrestrained epithelial growth. By adulthood, mammary glands in cycling virgin Tgfb1−/− mice were morphologically similar to those in Tgfb1+/+ and Tgfb1+/− animals, a normal branching pattern was observed, and the tissue differentiated into early alveolar structures in the diestrus phase of the ovarian cycle. Transplanted mammary gland epithelium showed a similar extent of ductal branching and evidence of secretory differentiation of luminal cells in pregnancy. These results reveal two opposing actions of TGFB1 during pubertal mammary gland morphogenesis, dependent on the cellular source of gene expression. When expressed in the epithelium, TGFB1 inhibits epithelial ductal growth, when expressed systemically, TGFB1 promotes epithelial ductal growth.

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.

Cellular Components of the Milk of the Tammar Wallaby (Macropus eugenii)

1997 ◽  
Vol 45 (4) ◽  
pp. 423 ◽  
Author(s):  
L. Young ◽  
K. Basden ◽  
D. W. Cooper ◽  
E. M. Deane
Keyword(s):  
Mammary Gland ◽  
Mononuclear Cells ◽  
Tammar Wallaby ◽  
Mammary Glands ◽  
Cell Type ◽  
Phagocytic Cells ◽  
Macropus Eugenii ◽  
Predominant Cell Type ◽  
Cellular Components

The cellular components of colostrum and milk of the tammar wallaby (Macropus eugenii) have been investigated over the period of oestrus, lactation and weaning. Macrophages, neutrophils, lymphocytes and other vacuolated mononuclear cells were identified. The total number and diversity of cells were higher in colostral secretions and in secretions from post-lactational mammary glands. Neutrophils were the predominant cell type in early secretions. Macrophages were more prevalent in the milk of animals that no longer had young attached to the teat. These observations are consistent with suggestions that phagocytic cells play a role in post-lactational repair of the mammary gland but also suggest that non-specific phagocytic protection plays a role in protection of the neonatal marsupial.

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.

The effect of bromocriptine on mammary-gland ultrastructure of hyperprolactinemic rats

1984 ◽  
Vol 42 ◽  
pp. 204-205
Author(s):  
I.C. Murray
Keyword(s):  
Mammary Gland ◽  
Dopamine Agonist ◽  
Alveolar Epithelium ◽  
Mammary Glands ◽  
Female Rats ◽  
Control Group ◽  
Cell Hyperplasia ◽  
Once Daily ◽  
Long Evans

In women, hyperprolactinemia is often due to a prolactin (PRL)-secreting adenoma or PRL cell hyperplasia. RRL excess stimulates the mammary glands and causes proliferation of the alveolar epithelium. Bromocriptine, a dopamine agonist, inhibits PRL secretion and is given to women to treat nonpuerperal galactorrhea. Old female rats have been reported to have PRL cell hyperplasia or adenoma leading to PRL hypersecretion and breast stimulation. Herein, we describe the effect of bromocriptine and consequently the reduction in serum PRL levels on the ultrastructure of rat mammary glands.Female Long-Evans rats, 23 months of age, were divided into control and bromocriptine-treated groups. The control animals were injected subcutaneously once daily with a 10% ethanol vehicle and were later divided into a normoprolactinemic control group with serum PRL levels under 30 ng/ml and a hyperprolactinemic control group with serum PRL levels above 30 ng/ml.

INTERACTIONS OF OESTRONE AND TESTOSTERONE ON MAMMARY GLANDS OF MALE RABBITS

1961 ◽  
Vol 36 (1) ◽  
pp. 141-156 ◽  
Author(s):  
B. Bengtsson ◽  
A. Norgren
Keyword(s):  
Mammary Gland ◽  
Testosterone Propionate ◽  
Mammary Glands ◽  
List Type ◽  
Stunted Growth ◽  
Abnormal Growth ◽  
Growth Reaction ◽  
Extensive Growth ◽  
Higher Doses

ABSTRACT The effect of testosterone and oestrone on the mammary glands of castrated male rabbits was studied. Testosterone propionate was used in daily doses from 0.5 to 80 mg. The doses of oestrone ranged from 0.05 to 25 μg per day. Mammary glands were examined after 14, 28 or 56 days of injections. 1) Testosterone in doses below 20 mg failed to affect the mammary glands. With 40 or 80 mg a distinct, though abnormal growth reaction was consistently obtained. 2) Oestrone in doses lower than 0.5 μg did not stimulate mammary growth. With 0.5 μg and higher doses extensive growth of the mammary glands occurred. Stunted growth and secretion were found in the mammary glands of rabbits injected with 12.5 or 25 μg oestrone. 3) Testosterone in doses of 1 or 5 to 10 mg depressed or abolished the response of the mammary glands to 0.5 μg oestrone. When testosterone, in doses ineffective when given alone, was added to at least 3.125 μg oestrone, the mammary glands developed alveoli. The abnormalities produced by the highest doses of oestrone studied were exaggerated by the addition of testosterone. 4) The observations indicate a complicated interplay between the actions of testosterone and oestrone on the mammary gland of the rabbit. The interactions between testosterone and oestrone are presumably different from those observed between progesterone and oestrone.

EFFECT OF LOCALLY IMPLANTED OESTROGEN ON THE RESPONSE OF THE RAT'S LACTATING MAMMARY GLAND TO OXYTOCIN

1973 ◽  
Vol 73 (4) ◽  
pp. 700-712 ◽  
Author(s):  
J. D. Bruce ◽  
X. Cofre ◽  
V. D. Ramirez
Keyword(s):  
Mammary Gland ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Recording System ◽  
Saline Infusion ◽  
High Dose ◽  
Low Doses ◽  
Milk Ejection ◽  
Lactating Mammary Gland ◽  
Small Rise

ABSTRACT On the day following delivery (day 1 of lactation) one abdominal mammary gland was implanted with oestrogen and the contralateral gland received an empty needle. At 2, 5 or 10 days of lactation the rats were anaesthetized with pentobarbital and the nipples of both abdominal glands were cannulated and their pressures recorded by means of transducers coupled to an amplifier and recording system. The normal mammary glands of 5-day lactating rats responded to very low doses of oxytocin (Syntocinon®, Sandoz) (5× 10−8 mU) with a rhythmic elevation in pressure. However, saline infusion also evoked a small rise in intra-mammary pressure. Earlier (2 days) and later (10 days) in lactation the responses were smaller. Oestrogen decreases significantly the milk ejection response to oxytocin, and the effect was maximal at day 10 of lactation. Histological observations confirmed the diminished reaction of the gland to oxytocin, since the milk was retained in the alveoli of rats bearing a mammary-oestrogen implant. A paradoxical rise in pressure was detected in normal as well as in oestrogen-implanted glands when the lowest dose of oxytocin was injected in lactating rats which had previously received a high dose of oxytocin (50 mU or 500 mU). These results reinforce the hypothesis that oestrogen alters the milk ejection response to oxytocin and that the mechanism is probably related to changes in the contractility of the myoepithelial cells.

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