Source:http://linkedlifedata.com/resource/pubmed/id/21613322
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
13
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| pubmed:dateCreated |
2011-6-9
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| pubmed:abstractText |
The mammalian kidney and male reproductive system are both derived from the intermediate mesoderm. The spatial and temporal expression of bone morphogenetic protein (BMP) 2 and BMP4 and their cognate receptor, activin like kinase 3 (ALK3), suggests a functional role for BMP-ALK3 signaling during formation of intermediate mesoderm-derivative organs. Here, we define cell autonomous functions for Alk3 in the kidney and male gonad in mice with CRE-mediated Alk3 inactivation targeted to intermediate mesoderm progenitors (Alk3(IMP null)). Alk3-deficient mice exhibit simple renal hypoplasia characterized by decreases in both kidney size and nephron number but normal tissue architecture. These defects are preceded by a decreased contribution of Alk3-deleted cells to the metanephric blastema and reduced expression of Osr1 and SIX2, which mark nephron progenitor cells. Mutant mice are also characterized by defects in intermediate mesoderm-derived genital tissues with fewer mesonephric tubules and testicular Leydig cells, epithelial vacuolization in the postnatal corpus epididymis, and decreased serum testosterone levels and reduced fertility. Analysis of ALK3-dependent signaling effectors revealed lineage-specific reduction of phospho-p38 MAPK in metanephric mesenchyme and phospho-SMAD1/5/8 in the testis. Together, these results demonstrate a requirement for Alk3 in distinct progenitor cell populations derived from the intermediate mesoderm.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
1477-9129
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
138
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2717-27
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| pubmed:meshHeading |
pubmed-meshheading:21613322-Androgens,
pubmed-meshheading:21613322-Animals,
pubmed-meshheading:21613322-Apoptosis,
pubmed-meshheading:21613322-Bone Morphogenetic Protein Receptors, Type I,
pubmed-meshheading:21613322-Cell Proliferation,
pubmed-meshheading:21613322-Fluorescent Antibody Technique,
pubmed-meshheading:21613322-Immunoblotting,
pubmed-meshheading:21613322-Immunohistochemistry,
pubmed-meshheading:21613322-In Situ Hybridization,
pubmed-meshheading:21613322-Kidney,
pubmed-meshheading:21613322-Male,
pubmed-meshheading:21613322-Mesoderm,
pubmed-meshheading:21613322-Mice,
pubmed-meshheading:21613322-Mice, Mutant Strains,
pubmed-meshheading:21613322-Models, Biological,
pubmed-meshheading:21613322-Nephrons,
pubmed-meshheading:21613322-Signal Transduction,
pubmed-meshheading:21613322-beta-Galactosidase
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| pubmed:year |
2011
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| pubmed:articleTitle |
Alk3 controls nephron number and androgen production via lineage-specific effects in intermediate mesoderm.
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| pubmed:affiliation |
Program in Developmental and Stem Cell Biology, Hospital for Sick Children, Toronto, ON M5G 1X8, Canada.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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