scholarly journals Role of FGF10/FGFR2b signaling during mammary gland development in the mouse embryo

Development ◽  
2002 ◽  
Vol 129 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Arnaud André Mailleux ◽  
Bradley Spencer-Dene ◽  
Christian Dillon ◽  
Delphine Ndiaye ◽  
Catherine Savona-Baron ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Mammary Gland Development ◽  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Fat Pad ◽  
Mammary Fat Pad ◽  
Gland Development ◽  
Mammary Placode ◽  
Dependent Pathway

The mouse develops five pairs of mammary glands that arise during mid-gestation from five pairs of placodes of ectodermal origin. We have investigated the molecular mechanisms of mammary placode development using Lef1 as a marker for the epithelial component of the placode, and mice deficient for Fgf10 or Fgfr2b, both of which fail to develop normal mammary glands. Mammary placode induction involves two different signaling pathways, a FGF10/FGFR2b-dependent pathway for placodes 1, 2, 3 and 5 and a FGF10/FGFR2b-independent pathway for placode 4. Our results also suggest that FGF signaling is involved in the maintenance of mammary bud 4, and that Fgf10 deficient epithelium can undergo branching morphogenesis into the mammary fat pad precursor.

scholarly journals Evidence That the Mammary Fat Pad Mediates the Action of Growth Hormone in Mammary Gland Development

Endocrinology ◽  
1998 ◽  
Vol 139 (2) ◽  
pp. 659-662 ◽  
Author(s):  
Paul D. Walden ◽  
Weifeng Ruan ◽  
Mark Feldman ◽  
David L. Kleinberg
Keyword(s):  
Growth Hormone ◽  
Mammary Gland ◽  
Mammary Gland Development ◽  
Fat Pad ◽  
Mammary Fat Pad ◽  
Gland Development

scholarly journals Nutritional Regulation of Mammary Gland Development and Milk Synthesis in Animal Models and Dairy Species

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 523
Author(s):  
Cathy Hue-Beauvais ◽  
Yannick Faulconnier ◽  
Madia Charlier ◽  
Christine Leroux
Keyword(s):  
Gene Expression ◽  
Molecular Mechanisms ◽  
Mammary Gland Development ◽  
Mammary Development ◽  
Feed Restriction ◽  
Nutritional Regulation ◽  
Milk Component ◽  
Lipid Supplementation ◽  
Gland Development

In mammals, milk is essential for the growth, development, and health. Milk quantity and quality are dependent on mammary development, strongly influenced by nutrition. This review provides an overview of the data on nutritional regulations of mammary development and gene expression involved in milk component synthesis. Mammary development is described related to rodents, rabbits, and pigs, common models in mammary biology. Molecular mechanisms of the nutritional regulation of milk synthesis are reported in ruminants regarding the importance of ruminant milk in human health. The effects of dietary quantitative and qualitative alterations are described considering the dietary composition and in regard to the periods of nutritional susceptibly. During lactation, the effects of lipid supplementation and feed restriction or deprivation are discussed regarding gene expression involved in milk biosynthesis, in ruminants. Moreover, nutrigenomic studies underline the role of the mammary structure and the potential influence of microRNAs. Knowledge from three lactating and three dairy livestock species contribute to understanding the variety of phenotypes reported in this review and highlight (1) the importance of critical physiological stages, such as puberty gestation and early lactation and (2) the relative importance of the various nutrients besides the total energetic value and their interaction.

scholarly journals Role of F-Box Protein βTrcp1 in Mammary Gland Development and Tumorigenesis

2004 ◽  
Vol 24 (18) ◽  
pp. 8184-8194 ◽  
Author(s):  
Yasusei Kudo ◽  
Daniele Guardavaccaro ◽  
Patricia G. Santamaria ◽  
Ryo Koyama-Nasu ◽  
Esther Latres ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Transgenic Mice ◽  
Mammary Gland Development ◽  
Mammary Glands ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Ductal Branching ◽  
F Box Protein ◽  
Gland Development

ABSTRACT The F-box protein βTrcp1 controls the stability of several crucial regulators of proliferation and apoptosis, including certain inhibitors of the NF-κB family of transcription factors. Here we show that mammary glands of βTrcp1−/− female mice display a hypoplastic phenotype, whereas no effects on cell proliferation are observed in other somatic cells. To investigate further the role of βTrcp1 in mammary gland development, we generated transgenic mice expressing human βTrcp1 targeted to epithelial cells under the control of the mouse mammary tumor virus (MMTV) long terminal repeat promoter. Compared to controls, MMTV βTrcp1 mammary glands display an increase in lateral ductal branching and extensive arrays of alveolus-like protuberances. The mammary epithelia of MMTV βTrcp1 mice proliferate more and show increased NF-κB DNA binding activity and higher levels of nuclear NF-κB p65/RelA. In addition, 38% of transgenic mice develop tumors, including mammary, ovarian, and uterine carcinomas. The targeting of βTrcp1 to lymphoid organs produces no effects on these tissues. In summary, our results support the notion that βTrcp1 positively controls the proliferation of breast epithelium and indicate that alteration of βTrcp1 function and expression may contribute to malignant behavior of breast tumors, at least in part through NF-κB transactivation.

scholarly journals Mammary Gland Development in Transgenic Male Mice Expressing Human P450 Aromatase

Endocrinology ◽  
2002 ◽  
Vol 143 (10) ◽  
pp. 4074-4083 ◽  
Author(s):  
Xiangdong Li ◽  
Anni Wärri ◽  
Sari Mäkelä ◽  
Tommi Ahonen ◽  
Tomi Streng ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Molecular Mechanisms ◽  
Mammary Gland Development ◽  
Hormone Receptors ◽  
Mammary Glands ◽  
Estrogen Receptor Α ◽  
Male Mice ◽  
Milk Protein Gene ◽  
Transgenic Mouse Strain ◽  
Gland Development

Abstract We recently generated a transgenic mouse strain that expresses the human aromatase gene under the ubiquitin C promoter (AROM+). We have previously shown that in these mice the serum estradiol concentration is highly elevated, whereas the testosterone concentration is decreased. In the present study we examined mammary gland development in AROM+ male mice at different ages and found that the mammary glands of AROM+ males undergo ductal and alveolar development morphologically resembling that of terminally differentiated female mammary glands, expressing mRNA for a milk protein gene (β-casein). The male mammary glands also express multiple hormone receptors typical for female mammary gland: estrogen receptor α and β, progesterone receptor, and PRL receptor. Furthermore, data showed activation of the Stat5 (signal transducer and activator of transcription 5) signaling pathway in the AROM+ male mammary gland. Interestingly, the phenotype observed is in part reversible. Treatment with finrozole, a specific aromatase inhibitor, caused an involution of the differentiated phenotype of the mammary gland, marked by the disappearance of alveolar structures and the majority of the tertiary side branches of the ducts. The present animal model is a valuable tool for better understanding the cellular and molecular mechanisms involved in the development of gynecomastia.

scholarly journals Long Intergenic Non-Coding RNAs in the Mammary Parenchyma and Fat Pad of Pre-Weaning Heifer Calves: Identification and Functional Analysis

Animals ◽  
2021 ◽  
Vol 11 (5) ◽  
pp. 1268
Author(s):  
Shengchao Zhang ◽  
Sibtain Ahmad ◽  
Yuxia Zhang ◽  
Guohua Hua ◽  
Jianming Yi
Keyword(s):  
Mammary Gland ◽  
Crude Protein ◽  
Regulatory Mechanism ◽  
Differentially Expressed ◽  
Milk Replacer ◽  
Rna Seq ◽  
Fat Pad ◽  
Mammary Fat Pad ◽  
Non Coding Rnas ◽  
Gland Development

Enhanced plane of nutrition at pre-weaning stage can promote the development of mammary gland especially heifer calves. Although several genes are involved in this process, long intergenic non-coding RNAs (lincRNAs) are regarded as key regulators in the regulated network and are still largely unknown. We identified and characterized 534 putative lincRNAs based on the published RNA-seq data, including heifer calves in two groups: fed enhanced milk replacer (EH, 1.13 kg/day, including 28% crude protein, 25% fat) group and fed restricted milk replacer (R, 0.45 kg/day, including 20% crude protein, 20% fat) group. Sub-samples from the mammary parenchyma (PAR) and mammary fat pad (MFP) were harvested from heifer calves. According to the information of these lincRNAs’ quantitative trait loci (QTLs), the neighboring and co-expression genes were used to predict their function. By comparing EH vs R, 79 lincRNAs (61 upregulated, 18 downregulated) and 86 lincRNAs (54 upregulated, 32 downregulated) were differentially expressed in MFP and PAR, respectively. In MFP, some differentially expressed lincRNAs (DELs) are involved in lipid metabolism pathways, while, in PAR, among of DELs are involved in cell proliferation pathways. Taken together, this study explored the potential regulatory mechanism of lincRNAs in the mammary gland development of calves under different planes of nutrition.

scholarly journals BAG3 contributes to HGF-mediated cell proliferation, migration, and invasion via the Egr1 pathway in gastric cancer

2018 ◽  
Vol 105 (1) ◽  
pp. 63-75
Author(s):  
Jae Chang Lee ◽  
Sung Ae Koh ◽  
Kyung Hee Lee ◽  
Jae-Ryong Kim
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cell Invasion ◽  
Molecular Mechanisms ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Protein Levels ◽  
Dependent Pathway

Introduction: Bcl2-associated athanogene 3 (BAG3) is elevated in several types of cancers. However, the role of BAG3 in progression of gastric cancer is unknown. Therefore, the present study aims to find out the role of BAG3 in hepatocyte growth factor (HGF)–mediated tumor progression and the molecular mechanisms by which HGF regulates BAG3 expression. Methods: BAG3 mRNA and protein were measured using reverse transcription polymerase chain reaction and Western blot in the 2 human gastric cancer cell lines, NUGC3 and MKN28, treated with or without HGF. The effects of BAG3 knockdown on cell proliferation, cell invasion, and apoptosis were analyzed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, the in vitro 2-chamber invasion assay, and flow cytometry in BAG3 short hairpin RNA (shRNA)–transfected cells and control cells. The signaling pathways involved in BAG3 that are regulated by HGF were analyzed. The chromatin immunoprecipitation assay was used to determine binding of Egr1 to the BAG3 promoter. Results: BAG3 mRNA and protein levels were increased following treatment with HGF. HGF-mediated BAG3 upregulation increased cell proliferation and cell invasion; however, it decreased apoptosis. HGF-mediated BAG3 upregulation is regulated by an ERK and Egr1-dependent pathway. BAG3 may have an important role in HGF-mediated cell proliferation and metastasis in gastric cancer through an ERK and Egr1-dependent pathway. Conclusion: This pathway may provide novel therapeutic targets and provide information for further identification of other targets of therapeutic significance in gastric cancer.

Progesterone receptor membrane component 1 is required for mammary gland development†

2020 ◽  
Vol 103 (6) ◽  
pp. 1249-1259
Author(s):  
Globinna Kim ◽  
Jong Geol Lee ◽  
Seung-A Cheong ◽  
Jung-Min Yon ◽  
Myeong Sup Lee ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Progesterone Receptor ◽  
Mammary Gland Development ◽  
Target Genes ◽  
Hormone Treatment ◽  
Mammary Glands ◽  
Membrane Component ◽  
Independent Manner ◽  
Receptor Membrane ◽  
Gland Development

Abstract The physiological functions of progesterone (P4) in female reproductive organs including the mammary glands are mediated via the progesterone receptor (PR), but not all P4 functions can be explained by PR-mediated signaling. Progesterone receptor membrane component 1 (PGRMC1), a potential mediator of P4 actions, plays an important role in the ovary and uterus in maintaining female fertility and pregnancy, but its function in mammary glands has not been elucidated. This study investigated the role of PGRMC1 in mouse mammary gland development. Unlike in the uterus, exogenous estrogen (E2) and/or P4 did not alter PGRMC1 expression in the mammary gland, and Pgrmc1-knockout (KO) mice displayed reduced ductal elongation and side branching in response to hormone treatment. During pregnancy, PGRMC1 was expressed within both the luminal and basal epithelium and gradually increased with gestation and decreased rapidly after parturition. Moreover, although lactogenic capacity was normal after parturition, Pgrmc1 KO resulted in defective mammary gland development from puberty until midpregnancy, while the expression of PR and its target genes was not significantly different between wild-type and Pgrmc1-KO mammary gland. These data suggest that PGRMC1 is essential for mammary gland development during puberty and pregnancy in a PR-independent manner.

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