ArticleThe American journal of pathology2005
Implication of Wt1 in the pathogenesis of nephrogenic failure in a mouse model of retinoic acid-induced caudal regression syndrome.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 30 citations in OpenAlex.
- Knockout of kdm4aa inhibits early embryonic development in zebrafish via downregulating cyp26a1.Molecular genetics and genomics : MGG · 2026Article
- Caudal Regression Syndrome-A Narrative Review: An Orthopedic Point of View.Children (Basel, Switzerland) · 2023Review
- Caudal regression syndrome and a pelvic kidney: case report.Anatomy & cell biology · 2020Article
- Perturbation of Retinoid Homeostasis Increases Malformation Risk in Embryos Exposed to Pregestational Diabetes.Diabetes · 2017Article
- A paradoxical teratogenic mechanism for retinoic acid.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Prenatal diagnosis of caudal regression syndrome without maternal diabetes mellitus.Journal of the Turkish German Gynecological Association · 2011Article
- Renal malformations associated with mutations of developmental genes: messages from the clinic.Pediatric nephrology (Berlin, Germany) · 2010Review
- Hyperglycemia: its imminent effects on mammalian nephrogenesis.Pediatric nephrology (Berlin, Germany) · 2005Review
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Authors and funding
8 authors at 4 institutions in 2 countries.
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Abstract
Renal malformations are common human birth defects that sometimes occur in the context of the caudal regression syndrome. Here, we found that exposure of pregnant mice to all-trans retinoic acid, at a time when the metanephros has yet to form, causes a failure of kidney development along with caudal regression. Maternal treatment with Am580 (retinoic acid receptor alpha agonist) also induced similar patterns of kidney maldevelopment in the fetus. In metanephroi from retinoic acid-treated pregnancies, renal mesenchyme condensed around the ureteric bud but then failed to differentiate into nephrons, instead undergoing involution by fulminant apoptosis to produce a renal agenesis phenotype. Results of whole organ cultures in serum-free medium, and also tissue recombination experiments, showed that the nephrogenic defect was intrinsic to the kidney and that it resided in the metanephric mesenchyme and not the ureteric bud. Renal mesenchyme from control embryos expressed Wilms' tumor 1 (Wt1), but this transcription factor, which is indispensable for kidney development, failed to express in metanephroi of retinoic acid-exposed embryos. Wt1 expression and organogenesis were both restored, however, when metanephroi from retinoic acid-treated pregnancies were grown in serum-containing media. Our data illuminate the pathobiology of a severe, teratogen-induced kidney malformation.
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