scholarly journals Enhanced Branching Morphogenesis in Mammary Glands of Mice Lacking Cell Surface β1,4-Galactosyltransferase

2002 ◽  
Vol 244 (1) ◽  
pp. 114-133 ◽  
Author(s):  
Kristin Steffgen ◽  
Kimberly Dufraux ◽  
Helen Hathaway
Keyword(s):  
Cell Surface ◽  
Branching Morphogenesis ◽  
Mammary Glands

scholarly journals Myosin II controls cellular branching morphogenesis and migration in three dimensions by minimizing cell-surface curvature

2015 ◽  
Vol 17 (2) ◽  
pp. 137-147 ◽  
Author(s):  
Hunter Elliott ◽  
Robert S. Fischer ◽  
Kenneth A. Myers ◽  
Ravi A. Desai ◽  
Lin Gao ◽  
...  
Keyword(s):  
Cell Surface ◽  
Myosin Ii ◽  
Branching Morphogenesis ◽  
Surface Curvature ◽  
Three Dimensions ◽  
And Migration

scholarly journals Overexpression of a Kinase-deficient Transforming Growth Factor-β Type II Receptor in Mouse Mammary Stroma Results in Increased Epithelial Branching

1999 ◽  
Vol 10 (4) ◽  
pp. 1221-1234 ◽  
Author(s):  
Heather Joseph ◽  
Agnieszka E. Gorska ◽  
Philip Sohn ◽  
Harold L. Moses ◽  
Rosa Serra
Keyword(s):  
Growth Factor ◽  
Transgenic Mice ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Dominant Negative ◽  
Type Ii ◽  
Ductal Epithelium ◽  
Lateral Branching

Members of the transforming growth factor-β (TGF-β) superfamily signal through heteromeric type I and type II serine/threonine kinase receptors. Transgenic mice that overexpress a dominant-negative mutation of the TGF-β type II receptor (DNIIR) under the control of a metallothionein-derived promoter (MT-DNIIR) were used to determine the role of endogenous TGF-βs in the developing mammary gland. The expression of the dominant-negative receptor was induced with zinc and was primarily localized to the stroma underlying the ductal epithelium in the mammary glands of virgin transgenic mice from two separate mouse lines. In MT-DNIIR virgin females treated with zinc, there was an increase in lateral branching of the ductal epithelium. We tested the hypothesis that expression of the dominant-negative receptor may alter expression of genes that are expressed in the stroma and regulated by TGF-βs, potentially resulting in the increased lateral branching seen in the MT-DNIIR mammary glands. The expression of hepatocyte growth factor mRNA was increased in mammary glands from transgenic animals relative to the wild-type controls, suggesting that this factor may play a role in TGF-β-mediated regulation of lateral branching. Loss of responsiveness to TGF-βs in the mammary stroma resulted in increased branching in mammary epithelium, suggesting that TGF-βs play an important role in the stromal–epithelial interactions required for branching morphogenesis.

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.

Conditional Knockout of Lgr4 Leads to Impaired Ductal Elongation and Branching Morphogenesis in Mouse Mammary Glands

2011 ◽  
Vol 5 (4) ◽  
pp. 205-212 ◽  
Author(s):  
K. Oyama ◽  
Y. Mohri ◽  
M. Sone ◽  
A. Nawa ◽  
K. Nishimori
Keyword(s):  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Conditional Knockout ◽  
Ductal Elongation

scholarly journals Matrix metalloproteinases are expressed during ductal and alveolar mammary morphogenesis, and misregulation of stromelysin-1 in transgenic mice induces unscheduled alveolar development.

1995 ◽  
Vol 6 (10) ◽  
pp. 1287-1303 ◽  
Author(s):  
J P Witty ◽  
J H Wright ◽  
L M Matrisian
Keyword(s):  
Basement Membrane ◽  
Transgenic Mice ◽  
Three Dimensional ◽  
Fold Increase ◽  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Stromal Fibroblasts ◽  
Alveolar Development ◽  
Ductal Branching

The matrix-degrading metalloproteinases stromelysin-1, stromelysin-3, and gelatinase A are expressed during ductal branching morphogenesis of the murine mammary gland. Stromelysin-1 expression in particular correlates with ductal elongation, and in situ hybridization and three-dimensional reconstruction studies revealed that stromelysin-1 mRNA was concentrated in stromal fibroblasts along the length of advancing ducts. Transgenic mice expressing an activated form of stromelysin-1 under the control of the MMTV promoter/enhancer exhibited inappropriate alveolar development in virgin females. Ultrastructural analysis demonstrated that the basement membrane underlying epithelial and myoepithelial cells was amorphous and discontinuous compared with the highly ordered basal lamina in control mammary glands. Transgenic mammary glands had at least a twofold increase in the number of cells/unit area and a 1.4-fold increase in the percent of cycling cells by 13 wk of age compared with nontransgenic littermates. In addition, transgenic glands expressed beta-casein mRNA, but not protein, and resembled the proliferative and differentiated state of an animal between 8 and 10 days pregnant. An analysis of metalloproteinase expression in the glands of normal pregnant females demonstrated that the same matrix metalloproteinase family members, including stromelysin-1, were expressed in connective tissue cells surrounding epithelial clusters during the time of lobuloalveolar development. These results suggest that metalloproteinases may assist in remodeling ECM during normal ductal and alveolar branching morphogenesis, and that disruption of the basement membrane by an activated metalloproteinase can affect basic cellular processes of proliferation and differentiation.

Overexpression of parathyroid hormone-related protein or parathyroid hormone in transgenic mice impairs branching morphogenesis during mammary gland development

Development ◽  
1995 ◽  
Vol 121 (11) ◽  
pp. 3539-3547 ◽  
Author(s):  
J.J. Wysolmerski ◽  
J.F. McCaughern-Carucci ◽  
A.G. Daifotis ◽  
A.E. Broadus ◽  
W.M. Philbrick
Keyword(s):  
Parathyroid Hormone ◽  
Transgenic Mice ◽  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Myoepithelial Cells ◽  
Breast Development ◽  
Related Protein ◽  
Amino Terminal ◽  
Parathyroid Hormone Related Protein ◽  
Breast Hypoplasia

Parathyroid hormone-related protein (PTHrP) was originally discovered as the tumor product that causes humoral hypercalcemia of malignancy. PTHrP is now known to be widely expressed in many normal fetal tissues where it may participate in the regulation of organogenesis. In this report, we document that overexpression of PTHrP in myoepithelial cells in the mammary glands of transgenic mice resulted in a form of breast hypoplasia characterized by a profound defect in branching morphogenesis of the developing mammary duct system. In addition, transgenic mice manifested a defect in lobuloalveolar development during pregnancy that seemed to be, in part, the consequence of an impaired ability to form terminal ducts in response to estrogen and progesterone stimulation. The effects of PTHrP on branching morphogenesis during breast development appeared to be the result of amino-terminal PTH-like sequences that signal through the PTH/PTHrP receptor, since overexpression of parathyroid hormone itself in the mammary glands of transgenic mice caused a similar development phenotype, and delivery of PTHrP (1–36) via locally implanted slow-release pellets impaired breast development in normal mice. These results suggest that PTHrP, which is a native product of mammary epithelial and myoepithelial cells may participate in normal breast development, perhaps as a locally secreted growth inhibitor.

scholarly journals Branching morphogenesis - historical first evidences

2020 ◽  
Vol 64 (7-8-9) ◽  
pp. 397-407
Author(s):  
Domenico Ribatti ◽  
Diego Guidolin
Keyword(s):  
Extracellular Matrix ◽  
Vascular System ◽  
Historical Review ◽  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Review Article ◽  
The Body ◽  
Matrix Cell ◽  
Branched Structures ◽  
Surrounding Extracellular Matrix

Branching morphogenesis, the creation of branched structures in the body, is a key feature of animal and plant development. It requires the coordinated interplay of multiple types of epithelial cells with the surrounding extracellular matrix. Cell migration, proliferation, and extracellular matrix dynamics have different roles in driving budding in different organs. This historical review article summarizes the first founding literature data concerning branching morphogenesis occurring in kidney, lung, vascular system, mammary glands and neurons.

scholarly journals Stromal–epithelial cell interactions and alteration of branching morphogenesis in macromastic mammary glands

2014 ◽  
Vol 18 (7) ◽  
pp. 1257-1266 ◽  
Author(s):  
Aimei Zhong ◽  
Guohua Wang ◽  
Jie Yang ◽  
Qijun Xu ◽  
Quan Yuan ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Branching Morphogenesis ◽  
Mammary Glands ◽  
Cell Interactions

Influence of Calcium Ions on the Plant Cell Surface: Membrane Fusions and Conformational Changes

1974 ◽  
Vol 32 ◽  
pp. 154-155
Author(s):  
D. James Morré ◽  
Charles E. Bracker ◽  
William J. VanDerWoude
Keyword(s):  
Cell Wall ◽  
Cell Surface ◽  
Conformational Changes ◽  
Calcium Ions ◽  
Surface Membrane ◽  
Carboxyl Groups ◽  
Cross Linking ◽  
Ultrastructural Evidence ◽  
Glycine Max L ◽  
Wall Extensibility

Calcium ions in the concentration range 5-100 mM inhibit auxin-induced cell elongation and wall extensibility of plant stems. Inhibition of wall extensibility requires that the tissue be living; growth inhibition cannot be explained on the basis of cross-linking of carboxyl groups of cell wall uronides by calcium ions. In this study, ultrastructural evidence was sought for an interaction of calcium ions with some component other than the wall at the cell surface of soybean (Glycine max (L.) Merr.) hypocotyls.

Basal Lamina Formation in DMBA Induced Mammary Carcinoma

1977 ◽  
Vol 35 ◽  
pp. 534-535
Author(s):  
I. Russo ◽  
J. Saby ◽  
J. Russo
Keyword(s):  
Mammary Carcinoma ◽  
Virgin Female ◽  
Mammary Glands ◽  
Sesame Oil ◽  
Female Rats ◽  
Ultrastructural Changes ◽  
Post Inoculation ◽  
Intermediate Type ◽  
Sprague Dawley ◽  
Intercellular Spaces

It has been previously demonstrated that DMBA-induced rat mammary carcinoma originates in the terminal end bud (TEB) of the mammary gland by proliferation of intermediate type cells (1). The earliest lesion identified is the intraductal proliferation (IDP), which gives rise to intraductal carcinomas. These evolve to cribriform, papillary and comedo types (2). In the present work, we report the ultrastructural changes that take place in the IDP for the formation of a cribriform pattern.Fifty-five-day-old Sprague Dawley virgin female rats were inoculated intra- gastrically with 20 mg 7,12-dimethylbenz(a)anthracene (DMBA) in 1 ml sesame oil. Non-inoculated, age-matched females were used as controls. Mammary glands from both control and experimental rats were removed weekly from the time of inoculation until 86 days post-inoculation. The glands were fixed and processed for electron microscopy (2).The first change observed in IDP's was the widening of intercellular spaces and the secretion of an electron dense material into these spaces (Fig. 1).

Sign in / Sign up

Export Citation Format

Share Document