Open AccessNeonatal calyceal dilation and renal fibrosis resulting from loss of Adamts-1 in mouse kidney is due to a developmental dysgenesis
Author(s) -
L. Mittaz,
Sharon D. Ricardo,
Gonzalo MartínezRodríguez,
I. Kola,
Darren J. Kelly,
Melissa H. Little,
Paul J. Hertzog,
Melanie Pritchard
Publication year - 2004
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfh603
Subject(s) - adamts , kidney , medicine , thrombospondin , in situ hybridization , immunohistochemistry , endocrinology , fibrosis , kidney development , pathology , metalloproteinase , biology , matrix metalloproteinase , messenger rna , biochemistry , embryonic stem cell , gene
A disintegrin and metalloproteinase with thrombospondin motifs 1, Adamts-1, is important for the development and function of the kidney. Mice lacking this protein present with renal lesions comprising enlarged calyces, and reduced cortex and medulla layers. Our current findings are consistent with the defect occurring due to a developmental dysgenesis.
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