scholarly journals Expression of xanthine oxidoreductase in mouse mammary epithelium during pregnancy and lactation: regulation of gene expression by glucocorticoids and prolactin

1996 ◽  
Vol 319 (3) ◽  
pp. 801-810 ◽  
Author(s):  
Mami KUROSAKI ◽  
Stefania ZANOTTA ◽  
Marco LI CALZI ◽  
Enrico GARATTINI ◽  
Mineko TERAO
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Regulation Of Gene Expression ◽  
Mammary Epithelium ◽  
Receptor Activation ◽  
Normal Breast ◽  
Enzymic Activity ◽  
Alveolar Epithelial Cells ◽  
Xanthine Oxidoreductase ◽  
Normal Breast Epithelium

In the mammary gland of virgin mice, xanthine oxidoreductase (XOR) enzymic activity is barely measurable. A high increase in the levels of the enzyme is observed during the last days of pregnancy and during lactation, and this is parallelled by an elevation in the amounts of the respective protein and transcript. In situ hybridization experiments demonstrate that the XOR mRNA is specifically expressed in the alveolar epithelial cells of the mammary gland. In HC11 cells, a model culture system for normal breast epithelium, the levels of XOR enzymic activity are dose- and time-dependently induced by dexamethasone, and a further synergistic augmentation is observed in the presence of dexamethasone plus prolactin. Increased XOR gene expression is consequent on glucocorticoid receptor activation, as indicated by sensitivity to the specific receptor antagonist RU486. In addition, the phenomenon is likely to involve protein phosphorylation and dephosphorylation events, as suggested by modulation of XOR mRNA by tyrosine kinase and phosphatase inhibitors.

scholarly journals Gene expression abnormalities in histologically normal breast epithelium of breast cancer patients

2007 ◽  
Vol 122 (7) ◽  
pp. 1557-1566 ◽  
Author(s):  
Anusri Tripathi ◽  
Chialin King ◽  
Antonio de la Morenas ◽  
Victoria Kristina Perry ◽  
Bohdana Burke ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Cancer Patients ◽  
Normal Breast ◽  
Breast Cancer Patients ◽  
Breast Epithelium ◽  
Normal Breast Epithelium

scholarly journals Pre-diagnostic role of platelet miRNA in coronary heart disease of healthy overweight subjects via platelet leptin receptor activation

2019 ◽  
Vol 6 (6) ◽  
pp. 3248-3261
Author(s):  
Yakubu Abdulrahman ◽  
Azrina Azlan ◽  
Loh Su Peng ◽  
Sabariah Md Noor
Keyword(s):  
Gene Expression ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Leptin Receptor ◽  
Regulation Of Gene Expression ◽  
Receptor Activation ◽  
Related Disorder ◽  
Treatment And Prevention ◽  
Effective Diagnosis

Obesity and overweight have become a global problem that development of various coronary artery diseases (CAD), such as myocardial infarction, atherosclerosis and congestive heart failure. Effective diagnosis is needed for effective treatment and prevention, particularly in healthy overweight subject. Platelets is an important component of hemostatic balance, that maintains the coagulation physiology. Platelets are involved in different pathological events such as thrombosis and CAD in various inflammatory conditions. There are evidences that highlight an important role of miRNA in regulation of gene expression profiling in platelets. Current hypothesis has shown the likelihood of using miRNAs as diagnostic markers in the event of CAD. This review article describes the association between overweight/obesity and platelets activation in elucidating the gene expression profiling in platelet miRNAs in CAD patient. The application of platelet miRNAs as predictive markers in overweight/obese individuals may become a marginal milestone in the history of this diet-related disorder treatment.  

scholarly journals Glucocorticoid-Induced Impairment of Mammary Gland Involution Is Associated with STAT5 and STAT3 Signaling Modulation

Endocrinology ◽  
2010 ◽  
Vol 151 (12) ◽  
pp. 5730-5740 ◽  
Author(s):  
Paola Y. Bertucci ◽  
Ana Quaglino ◽  
Andrea G. Pozzi ◽  
Edith C. Kordon ◽  
Adali Pecci
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Epithelial Cell ◽  
Target Genes ◽  
Cellular Proliferation ◽  
Mammary Epithelium ◽  
Hormone Treatment ◽  
Signal Transducer ◽  
Stat3 Signaling ◽  
Epithelial Cell Apoptosis

The mammary epithelium undergoes cyclical periods of cellular proliferation, differentiation, and regression. During lactation, the signal transducer and activator of transcription factor (STAT)-5A and the glucocorticoid receptor (GR) synergize to induce milk protein expression and also act as survival factors. During involution, STAT3 activation mediates epithelial cell apoptosis and mammary gland remodeling. It has been shown that the administration of glucocorticoids at weaning prevents epithelial cell death, probably by extracellular matrix breakdown prevention. Our results show that the synthetic glucocorticoid dexamethasone (DEX) modulates STAT5A and STAT3 signaling and inhibits apoptosis induction in postlactating mouse mammary glands, only when administered within the first 48 h upon cessation of suckling. DEX administration right after weaning delayed STAT5A inactivation and degradation, preserving gene expression of target genes as β-casein (bcas) and prolactin induced protein (pip). Weaning-triggered GR down-regulation is also delayed by the hormone treatment. Moreover, DEX administration delayed STAT3 activation and translocation into epithelial cells nuclei. In particular, DEX treatment impaired the increment in gene expression of signal transducer subunit gp130, normally up-regulated from lactation to involution and responsible for STAT3 activation. Therefore, the data shown herein indicate that glucocorticoids are able to modulate early involution by controlling the strong cross talk that GR, STAT5, and STAT3 pathways maintains in the mammary epithelium.

scholarly journals Regulation of Gene Expression in the Bovine Mammary Gland by Ovarian Steroids

2007 ◽  
Vol 90 ◽  
pp. E55-E65 ◽  
Author(s):  
E.E. Connor ◽  
M.J. Meyer ◽  
R.W. Li ◽  
M.E. Van Amburgh ◽  
Y.R. Boisclair ◽  
...  
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Regulation Of Gene Expression ◽  
Bovine Mammary Gland ◽  
Ovarian Steroids

Gene expression abnormalities in histologically normal breast epithelium from patients with luminal type of breast cancer

2014 ◽  
Vol 42 (5) ◽  
pp. 977-988 ◽  
Author(s):  
Pavol Zubor ◽  
Jozef Hatok ◽  
Petra Moricova ◽  
Karol Kajo ◽  
Ivana Kapustova ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Gene Expression ◽  
Normal Breast ◽  
Breast Epithelium ◽  
Normal Breast Epithelium ◽  
Luminal Type

Progesterone and EGF inhibit mouse mammary gland prolactin receptor and beta-casein gene expression

1994 ◽  
Vol 267 (5) ◽  
pp. C1467-C1472 ◽  
Author(s):  
S. Nishikawa ◽  
R. C. Moore ◽  
N. Nonomura ◽  
T. Oka
Keyword(s):  
Gene Expression ◽  
Mammary Gland ◽  
Prolactin Receptor ◽  
Mammary Epithelium ◽  
Mouse Mammary Gland ◽  
Mrna Levels ◽  
Casein Gene ◽  
Beta Casein

Regulation of mouse mammary gland long-form prolactin receptor (PRL-RL) mRNA levels by progesterone and epidermal growth factor (EGF) and the relationship between PRL-RL and beta-casein gene expression were examined in vivo and in vitro. PRL-RL and beta-casein mRNA levels increased approximately 6- and 15-fold from the pregnant to the lactating period, respectively, when normalized to the level of beta-actin mRNA. Ovariectomy of pregnant mice rapidly reduced the serum concentration of progesterone and increased the level of PRL-RL and beta-casein mRNAs approximately three- and fourfold compared with sham-operated animals 24 h after the operation. Injection of progesterone, but not estrogen, inhibited the increase in both mRNA levels. PRL-RL and beta-casein mRNA levels in cultured mammary epithelium increased in response to insulin, hydrocortisone, and prolactin, whereas progesterone or EGF caused inhibition. The combination of EGF and progesterone produced a greater inhibition than either hormone alone. These results indicate that both progesterone and EGF serve as negative regulators of lactogenesis.

scholarly journals Regulation of gene expression in human mammary epithelium: effect of breast pumping

2007 ◽  
Vol 195 (3) ◽  
pp. 503-511 ◽  
Author(s):  
Patricia D Maningat ◽  
Partha Sen ◽  
Agneta L Sunehag ◽  
Darryl L Hadsell ◽  
Morey W Haymond
Keyword(s):  
Gene Expression ◽  
Mrna Expression ◽  
Milk Fat ◽  
Regulation Of Gene Expression ◽  
Mammary Epithelium ◽  
Mammary Tissue ◽  
Lactating Women ◽  
Breast Pumping ◽  
Plasma Prl

Little is known of the molecular regulation of human milk production because of limitations in obtaining mammary tissue from lactating women. Our objectives were to evaluate whether RNA isolated from breast milk fat globules (MFGs) could be an alternative to mammary biopsies and to determine whether intense breast pumping, which increases prolactin (PRL) secretion, will upregulate α-lactalbumin (α-LA, a major determinant of lactose synthesis) transcription. RNA was isolated from MFG and transcripts of interest were identified and quantitated by real-time RT-PCR using an external standard for normalization. In addition, we performed microarray studies to determine MFG RNA gene expression profile. Ten lactating women were studied using two protocols: protocol A with intense pumping from 0800 to 0814 h followed by short pumping and protocol B with intense pumping from 1200 to 1214 h preceded by short pumping. Plasma PRL and MFG α-LA mRNA expression were measured. During protocol A, plasma PRL (61±7–248±43 μg/l by 14 min) and α-LA (3.5±0.9 fold by 6 h; P<0.03) increased. During protocol B, PRL gradually increased over 4 h from 69±14 to 205±28 μg/l, and further to 329±23 μg/l by 12 min of intense pumping; α-LA mRNA expression did not increase significantly. We conclude that MFGs provide a unique source to study the in vivo regulation of gene expression in mammary epithelial cells. α-LA mRNA is abundant in the MFG and its expression may be regulated by hormonal and temporal factors.

scholarly journals HSD17B1 expression induces inflammation-aided rupture of mammary gland myoepithelium

2018 ◽  
Vol 25 (4) ◽  
pp. 393-406 ◽  
Author(s):  
Päivi Järvensivu ◽  
Taija Heinosalo ◽  
Janne Hakkarainen ◽  
Pauliina Kronqvist ◽  
Niina Saarinen ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Mammary Gland ◽  
Mammary Tumorigenesis ◽  
Mammary Epithelium ◽  
Receptor Activation ◽  
Serum Prolactin ◽  
Mammary Gland Tissue ◽  
Highly Active ◽  
Gland Tissue

Hydroxysteroid (17-beta) dehydrogenase type 1 (HSD17B1) converts low-active estrogen estrone to highly active estradiol. Estradiol is necessary for normal postpubertal mammary gland development; however, elevated estradiol levels increase mammary tumorigenesis. To investigate the significance of the human HSD17B1 enzyme in the mammary gland, transgenic mice universally overexpressing human HSD17B1 were used (HSD17B1TG mice). Mammary glands obtained from HSD17B1TG females at different ages were investigated for morphology and histology, and HSD17B1 activity and estrogen receptor activation in mammary gland tissue were assessed. To study the significance of HSD17B1 enzyme expression locally in mammary gland tissue, HSD17B1-expressing mammary epithelium was transplanted into cleared mammary fat pads of wild-type females, and the effects on mammary gland estradiol production, epithelial cells and the myoepithelium were investigated. HSD17B1TG females showed increased estrone to estradiol conversion and estrogen-response element-driven estrogen receptor signaling in mammary gland tissue, and they showed extensive lobuloalveolar development that was further enhanced by age along with an increase in serum prolactin concentrations. At old age, HSD17B1TG females developed mammary cancers. Mammary-restricted HSD17B1 expression induced lesions at the sites of ducts and alveoli, accompanied by peri- and intraductal inflammation and disruption of the myoepithelial cell layer. The lesions were shown to be estrogen dependent, as treatment with an antiestrogen, ICI 182,780, starting when lesions were already established reversed the phenotype. These data elucidate the ability of human HSD17B1 to enhance estrogen action in the mammary glandin vivoand indicate that HSD17B1 is a factor inducing phenotypic alterations associated with mammary tumorigenesis.

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