Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1993-8-31
pubmed:abstractText
We describe the renal cystic disease occurring in a new inbred strain of mice which developed as a spontaneous mutation in otherwise healthy Balb/c mice. The disease displays characteristics of an autosomal recessive polycystic kidney disease. Affected animals develop massive cystic enlargement of the kidneys and die of renal failure at the age of 4 weeks. During postnatal development, there is a gradual shift in site of the lesions. At birth, cystic dilations are localized almost exclusively in proximal tubular segments, whereas in the terminal stages of the disease, 80% of the cysts are localized in collecting tubular segments as defined by segment specific lectin binding. The composition of the basement membrane of the cystic tubular walls during postnatal development as analyzed by immunocytochemistry is essentially normal during the earliest stage of cyst formation. However, with disease progression, the cystic tubular basement membrane demonstrates a decreased immunoreactivity to anti-laminin and anti-entactin antibodies. This indicates a shift in cyst localization during disease progression in this model, and suggests that basement membrane abnormalities are not a primary feature of the early cyst formation and progressive enlargement.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0385-2385
pubmed:author
pubmed:issnType
Print
pubmed:volume
35
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
349-54
pubmed:dateRevised
2011-8-1
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
A new murine model of autosomal recessive polycystic kidney disease.
pubmed:affiliation
Department of Pediatrics, Children's Hospital Medical Center and School of Medicine, University of Washington, Seattle.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.