Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-4-21
pubmed:abstractText
Deletion of the transcription factor CCAAT/enhancer binding protein (C/EBP)beta results in a severe inhibition of lobuloalveolar development in the mouse mammary gland. Because progesterone receptor (PR) is requisite for alveolar development, the expression of PR was investigated in C/EBPbeta-/- mice. Unexpectedly, the number of PR-positive cells, as well as the levels of PR mRNA, were elevated 3-fold in the mammary glands of C/EBPbeta-/- mice. Furthermore, in contrast to wild-type nulliparous mice, in which PR distribution shifted from a uniform to nonuniform pattern between 8-12 weeks of age, C/EBPbeta-/- mice exhibited uniform PR distribution throughout all stages of mammary development analyzed. No change in C/EBPbeta mRNA levels was observed in the mammary glands of PR-/- mice, suggesting that PR acts in a pathway either in parallel to or downstream of C/EBPbeta. The overexpression and disrupted cellular distribution of PR in C/EBPbeta-/- mice were coincident with a striking 10-fold decrease in cell proliferation after acute steroid hormone treatment, assayed by incorporation of bromodeoxyuridine. In wild-type mice, PR and bromodeoxyuridine-positive cells were adjacent to each other and rarely colocalized. No differences in the level or pattern of PR expression were observed in the uterus, suggesting that C/EBPbeta influences PR in a mammary-specific fashion. Together, these data suggest that C/EBPbeta may control cell fate decisions in the mammary gland through the appropriate temporal and spatial expression of molecular markers, such as PR, that induce the proliferation of alveolar progenitor cells via juxtacrine mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0888-8809
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
359-68
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10707954-Animals, pubmed-meshheading:10707954-Biological Markers, pubmed-meshheading:10707954-CCAAT-Enhancer-Binding Proteins, pubmed-meshheading:10707954-Cell Division, pubmed-meshheading:10707954-Cell Lineage, pubmed-meshheading:10707954-DNA Replication, pubmed-meshheading:10707954-DNA-Binding Proteins, pubmed-meshheading:10707954-Epithelial Cells, pubmed-meshheading:10707954-Female, pubmed-meshheading:10707954-Fluorescent Antibody Technique, Indirect, pubmed-meshheading:10707954-Gene Deletion, pubmed-meshheading:10707954-Gene Expression Regulation, Developmental, pubmed-meshheading:10707954-In Situ Hybridization, pubmed-meshheading:10707954-Mammary Glands, Animal, pubmed-meshheading:10707954-Mice, pubmed-meshheading:10707954-Mice, Inbred C57BL, pubmed-meshheading:10707954-Mice, Knockout, pubmed-meshheading:10707954-Nuclear Proteins, pubmed-meshheading:10707954-RNA, Messenger, pubmed-meshheading:10707954-Receptors, Progesterone
pubmed:year
2000
pubmed:articleTitle
C/EBPbeta (CCAAT/enhancer binding protein) controls cell fate determination during mammary gland development.
pubmed:affiliation
Department of Cell Biology, Baylor College of Medicine, Houston, Texas 77030-3498, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.