Document Detail


Apoptosis and involution in the mammary gland are altered in mice lacking a novel receptor, beta1,4-Galactosyltransferase I.
MedLine Citation:
PMID:  15282149     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Receptor-mediated cell-extracellular matrix (ECM) interactions are critical regulators of cell survival, and perturbing these signaling pathways can disrupt cellular differentiation and function in a variety of tissues, including the mammary gland. One such receptor is the cell surface-associated, long isoform of beta1,4-galactosyltransferase I (GalT I). Deletion of long GalT I leads to increased mammary ductal branching morphogenesis [Dev. Biol., 244 (2002) 114]. Here, we show that this expansion in the mammary epithelial (ME) cell compartment is accomplished through decreased apoptosis during pregnancy and involution. Decreased apoptosis during involution is concomitant with delayed alveolar collapse, persistent expression of the milk protein gene alpha-lactalbumin and delayed expression of genes associated with the tissue-remodeling phase of involution. Using 3-dimensional in vitro cultures, we show that the decrease in apoptosis is dependent on laminin 1, a ligand for surface GalT I, suggesting that surface GalT I negatively influences ECM-dependent cell survival, a novel function for an ECM receptor. In the best-studied examples, ECM promotes survival through integrin receptor-mediated activation of focal adhesion kinase (FAK). Aggregation of surface GalT I also activates FAK, therefore, we asked if FAK activation was altered in ME from long GalT I null mice. Activated FAK was appropriately localized to focal adhesions in long GalT I null ME. However, FAK activation was constitutively reduced 4.5-fold in long GalT I nulls relative to wild type. Expression of the integrin beta1 subunit was not affected by loss of long GalT I. Collectively, these results suggest that surface GalT I might negatively regulate ME cell survival by linking integrin-independent FAK activation to apoptotic rather than survival signaling events.
Authors:
Laura de la Cruz; Kristin Steffgen; Andrea Martin; Carli McGee; Helen Hathaway
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Developmental biology     Volume:  272     ISSN:  0012-1606     ISO Abbreviation:  Dev. Biol.     Publication Date:  2004 Aug 
Date Detail:
Created Date:  2004-07-29     Completed Date:  2004-10-04     Revised Date:  2014-09-24    
Medline Journal Info:
Nlm Unique ID:  0372762     Medline TA:  Dev Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  286-309     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD29 / metabolism
Apoptosis / physiology*
Cell Membrane / metabolism
Cells, Cultured
Epithelial Cells / metabolism
Extracellular Matrix / metabolism
Female
Focal Adhesion Kinase 1
Focal Adhesion Protein-Tyrosine Kinases
Galactosyltransferases / genetics*,  metabolism*
Isoenzymes / genetics,  metabolism
Lactalbumin / genetics
Lactation
Laminin / metabolism
Mammary Glands, Animal / pathology*,  physiology
Mice
Mice, Mutant Strains
Pregnancy
Pregnancy, Animal
Protein-Tyrosine Kinases / metabolism
Vinculin / metabolism
Grant Support
ID/Acronym/Agency:
1S10 RR14668/RR/NCRR NIH HHS; P20 RR11830/RR/NCRR NIH HHS; R24 CA88339/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD29; 0/Isoenzymes; 0/Laminin; 0/laminin 1; 125361-02-6/Vinculin; 9013-90-5/Lactalbumin; EC 2.4.1.-/Galactosyltransferases; EC 2.4.1.133/xylosylprotein 4-beta-galactosyltransferase; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.10.2/Focal Adhesion Kinase 1; EC 2.7.10.2/Focal Adhesion Protein-Tyrosine Kinases; EC 2.7.10.2/Ptk2 protein, mouse

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