scholarly journals Has the mammary gland a protective mechanism against overexposure to triiodothyronine during the peripartum period? The prolactin pulse down-regulates mammary type I deiodinase responsiveness to norepinephrine

2004 ◽  
Vol 183 (2) ◽  
pp. 267-277 ◽  
Author(s):  
B Anguiano ◽  
R Rojas-Huidobro ◽  
G Delgado ◽  
C Aceves
Keyword(s):  
Mammary Gland ◽  
Critical Role ◽  
Alveolar Epithelium ◽  
Late Pregnancy ◽  
Protective Mechanism ◽  
Type I ◽  
Key Factor ◽  
Pregnancy And Lactation ◽  
Contrary Effect ◽  
Peripartum Period

Peripartum is a crucial period for mammary gland final differentiation and the onset of lactation. Although the ‘trigger’ for lactogenesis depends on several hormones, a key factor is the peripartum prolactin (PRL) pulse whose deletion results in a failure to initiate milk production. Other hormones having a critical role during this period but exerting a contrary effect are the thyronines. A transitory hypothyroidism occurs at peripartum in serum and several other extrathyroidal tissues, whereas the induction of hyperthyroidism during late pregnancy is associated with the absence of lactation after delivery. We analyzed the mammary gland during pregnancy and lactation for: (a) the type and amount of thyroid receptors (TRs), (b) the local triiodothyronine (T3) generation catalyzed by type I deiodinase (Dio1), (c) the Dio1 response to norepinephrine (NE) and (d) the effect on Dio1 and TRs of blocking the PRL pulse at peripartum. Our data showed that during pregnancy the mammary gland contains Dio1 in low amounts associated with the highest expression of TRα1; whereas during lactation the gland shows high levels of both Dio1 and TRα1. However, at peripartum, both TRs and Dio1 decrease, and Dio1 becomes refractory to NE. This refractoriness disappears when the PRL pulse is blocked by the dopamine agonist bromocriptine. This blockade is also accompanied by a significant decrease in cyclin D1 expression. Our data suggested that the peripartum PRL pulse is part of a protective mechanism against precocious differentiation and/or premature involution of the alveolar epithelium due to T3 overexposure.

scholarly journals Collagen molecular phenotypic switch between non-neoplastic and neoplastic canine mammary tissues

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Masahiko Terajima ◽  
Yuki Taga ◽  
Becky K. Brisson ◽  
Amy C. Durham ◽  
Kotaro Sato ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Mammary Carcinoma ◽  
Cancer Biology ◽  
Type I Collagen ◽  
Critical Role ◽  
Premature Death ◽  
Mammary Tissue ◽  
Type I ◽  
Cross Links

AbstractIn spite of major advances over the past several decades in diagnosis and treatment, breast cancer remains a global cause of morbidity and premature death for both human and veterinary patients. Due to multiple shared clinicopathological features, dogs provide an excellent model of human breast cancer, thus, a comparative oncology approach may advance our understanding of breast cancer biology and improve patient outcomes. Despite an increasing awareness of the critical role of fibrillar collagens in breast cancer biology, tumor-permissive collagen features are still ill-defined. Here, we characterize the molecular and morphological phenotypes of type I collagen in canine mammary gland tumors. Canine mammary carcinoma samples contained longer collagen fibers as well as a greater population of wider fibers compared to non-neoplastic and adenoma samples. Furthermore, the total number of collagen cross-links enriched in the stable hydroxylysine-aldehyde derived cross-links was significantly increased in neoplastic mammary gland samples compared to non-neoplastic mammary gland tissue. The mass spectrometric analyses of type I collagen revealed that in malignant mammary tumor samples, lysine residues, in particular those in the telopeptides, were markedly over-hydroxylated in comparison to non-neoplastic mammary tissue. The extent of glycosylation of hydroxylysine residues was comparable among the groups. Consistent with these data, expression levels of genes encoding lysyl hydroxylase 2 (LH2) and its molecular chaperone FK506-binding protein 65 were both significantly increased in neoplastic samples. These alterations likely lead to an increase in the LH2-mediated stable collagen cross-links in mammary carcinoma that may promote tumor cell metastasis in these patients.

scholarly journals Expression of Prolactin mRNA in Rat Mammary Gland During Pregnancy and Lactation

2000 ◽  
Vol 48 (3) ◽  
pp. 389-395 ◽  
Author(s):  
Toshiki Iwasaka ◽  
Shinobu Umemura ◽  
Kochi Kakimoto ◽  
Haruko Koizumi ◽  
Yoshiyuki R. Osamura
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Late Pregnancy ◽  
Mammary Epithelial ◽  
Rt Pcr ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Pcr Method

We studied the expression of prolactin (PRL) mRNA in the mammary gland of resting, pregnant, lactating, and weanling rats using in situ and solution reverse transcriptase-polymerase chain reaction (RT-PCR). In mid- to late pregnancy and throughout lactation, PRL mRNA was detected in both in situ and solution RT-PCR. These PRL mRNA signals were clearly identified in the cytoplasm of alveolar and ductal mammary epithelial cells by the in situ RT-PCR method. In mid- to late pregnancy, such as at the initiating point of PRL mRNA expression, we confirmed in some cases a lack of PRL mRNA by solution RT-PCR. In addition, in the early weaning phase, no signals were detected by solution RT-PCR. However, slight focal signals were detected in some poorly vacuolated cytoplasm of regressing acinar cells by in situ RT-PCR. These findings suggest that PRL mRNA in rat mammary gland begins in mid- to late pregnancy in parallel with the development of the mammary gland, continues throughout lactation, and declines in the early phase of weaning, with regression of mammary epithelial cells.

Mammary gland function and development: effect of zinc deficiency in rat

1980 ◽  
Vol 238 (1) ◽  
pp. E26-E31 ◽  
Author(s):  
P. B. Mutch ◽  
L. S. Hurley
Keyword(s):  
Mammary Gland ◽  
Zinc Deficiency ◽  
Dna Content ◽  
Late Pregnancy ◽  
Female Rats ◽  
Deficient Diet ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Gland Function ◽  
Zinc Deficient Diet

The effect of dietary zinc deficiency during late pregnancy and lactation on the rat mammary gland was investigated by feeding female rats either a zinc-deficient diet (0.4 ppm Zn) or a zinc-sufficient diet (100 ppm Zn) ad libitum or restricted in amount. Zinc deficiency from day 0 of lactation specifically reduced the total RNA content of lactating mammary glands on day 14, but had no effect beyond that of food restriction on their total DNA content, Both RNA and DNA content of the mammary gland were decreased by reduced food intake. Zinc deficiency from day 14 of pregnancy to day 2 of lactation severely impaired parturition and prevented the normal rise in mammary gland RNA seen during lactogenesis in control animals. A shorter deficiency period, from day 18 of gestation, had no effect on mammary gland nucleic acids other than that due to inanition.

scholarly journals Transcript abundances of the prolactin receptor, the leptin receptor and their major suppressor in the sheep mammary gland during pregnancy and lactation

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Malgorzata Szczesna ◽  
Katarzyna Kirsz ◽  
Michal Nowakowski ◽  
Dorota A. Zieba
Keyword(s):  
Mammary Gland ◽  
Leptin Receptor ◽  
Prolactin Receptor ◽  
Signal Transduction Pathway ◽  
Late Pregnancy ◽  
Transcript Level ◽  
Transcript Abundance ◽  
Cytokine Signaling ◽  
Pregnancy And Lactation ◽  
Plasma Prl

AbstractThis study aimed to expand the knowledge of the interactions between prolactin (PRL) and leptin in the ovine mammary gland during pregnancy and lactation; we examined the mRNA expression of prolactin receptor (PRLR), the long form of the leptin receptor (LRb) and suppressor of cytokine signaling (SOCS)-3 in mammary gland biopsies collected on days 60, 90 and 120 of pregnancy and on days 30, 60 and 90 of lactation (n = 6 for each time point), along with the plasma PRL and leptin concentrations. The PRL concentrations were stable throughout pregnancy and increased during lactation. The plasma leptin concentrations were comparable among nonpregnant, early-pregnant, late-pregnant and lactating ewes, but this metric peaked during mid-pregnancy. Expression of PRLR and SOCS-3 in the mammary gland fluctuated during the transition from pregnancy to lactation, and differences in LRb expression occurred during the late stages of lactation. The LRb transcript abundance was approximately 31 times higher in ewes on day 60 of lactation than in early-lactating ewes. Expression of SOCS-3 mRNA in biopsies gradually decreased over the course of pregnancy and reached a minimum value during late pregnancy. After lambing, the transcript level of SOCS-3 increased and peaked on day 60 of lactation. During pregnancy, the plasma PRL concentration positively correlated with the abundances of PRLR (r = 0.971, P < 0.01) and SOCS-3 (r = 0.818, P < 0.05). Positive correlations were also observed between the transcript abundances of SOCS-3 and LRb (r = 0.854, P < 0.05). The variations observed in the plasma PRL and leptin concentrations and the changes in expression of key leptin and PRL signal transduction pathway components, such as PRLR, LRb and SOCS-3, indicate that the efficacies of both hormone actions are modulated in a multilevel manner throughout pregnancy and lactation. These interactions may regulate the ability of the mammary gland to respond to current energy requirements and challenges, thus affecting milk yield and lactation duration.

Ultrasonographic assessment of the feline mammary gland

2008 ◽  
Vol 10 (5) ◽  
pp. 466-471 ◽  
Author(s):  
Rita Payan-Carreira ◽  
Ana C. Martins-Bessa
Keyword(s):  
Mammary Gland ◽  
Diagnostic Tool ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Mammary Tissue ◽  
Physiological Changes ◽  
Linear Transducer ◽  
Pregnancy And Lactation ◽  
Ultrasonographic Assessment ◽  
Ultrasonographic Appearance

The aim of this study is to characterise the feline mammary echotexture using B-mode ultrasonography, which is not routinely used to examine the feline mammary gland. Using a 5–9 MHz linear transducer the ultrasonographic appearance of non-stimulated and stimulated mammary glands was determined in 35 mature intact non-pregnant, pregnant and lactating queens aged from 16 months to 8 years. In intact non-pregnant queens, mammary glands are fairly underdeveloped and on the ultrasonograms they appear with a regular hypoechoic texture and generally show a thickness of less than 2.0 mm. The stimulated mammary tissue typically presents a more hyperechoic appearance compared to the non-stimulated gland and a fine granular echotexture. Maximum echogenicity of the mammary gland is reached during lactation. In late pregnancy, the mammary glands reach 6–9 mm in thickness. During lactation, the size of the glands depends on the existence of a suckling stimulus, with the suckled glands reaching about 11 mm in thickness. Ductal structures can only be imaged during late pregnancy and lactation. Ultrasonographic evaluation of the feline mammary gland can become a valuable diagnostic tool to characterise physiological changes and may further contribute to a better characterisation of diseased mammary tissue.

scholarly journals Polyamine biogenesis in the rat mammary gland during pregnancy and lactation

1972 ◽  
Vol 130 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Diane H. Russell ◽  
Thomas A. McVicker
Keyword(s):  
Mammary Gland ◽  
Late Pregnancy ◽  
Normal Mammary Gland ◽  
Biosynthetic Activity ◽  
A Value ◽  
Lactating Mammary Gland ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Gland Development ◽  
Very High

Polyamines and RNA accumulate in the rat mammary gland during pregnancy, but the major increases occur after parturition. Therefore the major increases occur after the gland has obtained its maximal complement of epithelial cells. During lactation, the spermidine concentration rises above 5mm and RNA content in the lactating mammary gland reaches a value 16 times that of the unstimulated mammary gland. The ratio of spermidine/spermine, an increase of which initially signals an elevation in biosynthetic activity, is near 1 in the normal mammary gland and is greater than 10 in the lactating mammary gland. Putrescine concentration is very low during the entire course of mammary-gland development, with the exception of early pregnancy. The low putrescine concentration probably reflects the very rapid conversion of putrescine into spermidine. Both ornithine decarboxylase, the enzyme that synthesizes putrescine, and putrescine-stimulated S-adenosyl-l-methionine decarboxylase, the enzyme that synthesizes spermidine, increase in activity during middle and late pregnancy; during lactation, both enzyme activities are elevated until the 21st day of lactation, and then decline. These declines are concomitant with involution. Also, it was found that the amount of ribonuclease activity in the mammary gland was very high during lactation, almost double that in the gland during pregnancy.

scholarly journals Identification of reference genes for RT-qPCR in ovine mammary tissue during late pregnancy and lactation and in response to maternal nutritional programming

2014 ◽  
Vol 46 (15) ◽  
pp. 560-570 ◽  
Author(s):  
A. M. Paten ◽  
S. J. Pain ◽  
S. W. Peterson ◽  
H. T. Blair ◽  
P. R. Kenyon ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Reference Genes ◽  
Physiological State ◽  
Late Pregnancy ◽  
Mammary Tissue ◽  
Qpcr Data ◽  
Maternal Programming ◽  
Pregnancy And Lactation ◽  
Measure Gene Expression

The mammary gland is a complex tissue consisting of multiple cell types which, over the lifetime of an animal, go through repeated cycles of development associated with pregnancy, lactation and involution. The mammary gland is also known to be sensitive to maternal programming by environmental stimuli such as nutrition. The molecular basis of these adaptations is of significant interest, but requires robust methods to measure gene expression. Reverse-transcription quantitative PCR (RT-qPCR) is commonly used to measure gene expression, and is currently the method of choice for validating genome-wide expression studies. RT-qPCR requires the selection of reference genes that are stably expressed over physiological states and treatments. In this study we identify suitable reference genes to normalize RT-qPCR data for the ovine mammary gland in two physiological states; late pregnancy and lactation. Biopsies were collected from offspring of ewes that had been subjected to different nutritional paradigms during pregnancy to examine effects of maternal programming on the mammary gland of the offspring. We evaluated eight candidate reference genes and found that two reference genes ( PRPF3 and CUL1) are required for normalising RT-qPCR data from pooled RNA samples, but five reference genes are required for analyzing gene expression in individual animals ( SENP2, EIF6, MRPL39, ATP1A1, CUL1). Using these stable reference genes, we showed that TET1, a key regulator of DNA methylation, is responsive to maternal programming and physiological state. The identification of these novel reference genes will be of utility to future studies of gene expression in the ovine mammary gland.

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.

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