Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1998-12-11
pubmed:abstractText
Prolactin induces mammopoiesis and lactogenesis through the Janus kinase-signal transducers and activators of transcription pathway, with Stat5a being a principal and obligate cytoplasmic and nuclear signaling molecule. Mice from which the Stat5a gene has been deleted fail to develop functional mammary tissue during their first pregnancy. Lobuloalveolar outgrowth is curtailed, and epithelial cells fail to progress to functional differentiation. Here, we investigate whether the effect of Stat5a deficiency is restricted to the epithelium and whether the gland has the capacity to activate alternative signaling pathways that could restore development and function. Mammary gland transplant experiments showed that Stat5a-deficient epithelium does not differentiate in wild-type stroma, thus demonstrating a cell-autonomous role for Stat5a. The capacity of Stat5a-deficient mammary tissue to develop and secrete milk was measured after consecutive pregnancies and with postpartum suckling. Neither of these regimens could independently restore lactation. However, the combination of several pregnancies and suckling stimuli resulted in a partial establishment of lactation and an increase of Stat5b activity. These experiments demonstrate that the mammary gland has inherent plasticity that allows it to use different signals to achieve its ultimate purpose, the production of milk to nurture newborn offspring.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1044-9523
pubmed:author
pubmed:issnType
Print
pubmed:volume
9
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
795-803
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:9751123-Animals, pubmed-meshheading:9751123-Animals, Newborn, pubmed-meshheading:9751123-Animals, Suckling, pubmed-meshheading:9751123-Cell Division, pubmed-meshheading:9751123-DNA-Binding Proteins, pubmed-meshheading:9751123-Epithelial Cells, pubmed-meshheading:9751123-Epithelium, pubmed-meshheading:9751123-Female, pubmed-meshheading:9751123-Humans, pubmed-meshheading:9751123-Lactation, pubmed-meshheading:9751123-Male, pubmed-meshheading:9751123-Mammary Glands, Animal, pubmed-meshheading:9751123-Mice, pubmed-meshheading:9751123-Milk Proteins, pubmed-meshheading:9751123-Pregnancy, pubmed-meshheading:9751123-STAT5 Transcription Factor, pubmed-meshheading:9751123-Signal Transduction, pubmed-meshheading:9751123-Trans-Activators, pubmed-meshheading:9751123-Tumor Suppressor Proteins
pubmed:year
1998
pubmed:articleTitle
Functional rescue of Stat5a-null mammary tissue through the activation of compensating signals including Stat5b.
pubmed:affiliation
Laboratory of Genetics and Physiology, National Institutes of Diabetes, Digestive and Kidney Diseases, NIH, Bethesda, Maryland 20892, USA.
pubmed:publicationType
Journal Article