ArticleAmerican journal of physiology. Renal physiology2009
Deficiency in Six2 during prenatal development is associated with reduced nephron number, chronic renal failure, and hypertension in Br/+ adult mice.
Article in American journal of physiology. Renal physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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21 citing papers in PubMed, 45 citations in OpenAlex.
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- Discovery of gene-alcohol interaction loci influencing blood pressure in 1.1 million individuals from multiple populations.Research square · 2026Article
- Lysine-specific demethylase 1a is obligatory for gene regulation during kidney development.bioRxiv : the preprint server for biology · 2025Article
- Impact of gestational low-protein intake on embryonic kidney microRNA expression and in nephron progenitor cells of the male fetus.PloS one · 2021Article
- Renal developmental genes are differentially regulated after unilateral ureteral obstruction in neonatal and adult mice.Scientific reports · 2020Article
- The exocyst complex regulates insulin-stimulated glucose uptake of skeletal muscle cells.American journal of physiology. Endocrinology and metabolism · 2019Article
- Lin28 and let-7 regulate the timing of cessation of murine nephrogenesis.Nature communications · 2019Article
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- Magnetic susceptibility anisotropy outside the central nervous system.NMR in biomedicine · 2017Review
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- Fibroproliferative response to urothelial failure obliterates the ureter lumen in a mouse model of prenatal congenital obstructive nephropathy.Scientific reports · 2016Article
- A new frontonasal dysplasia syndrome associated with deletion of the SIX2 gene.American journal of medical genetics. Part A · 2016Article
- Urothelial Defects from Targeted Inactivation of Exocyst Sec10 in Mice Cause Ureteropelvic Junction Obstructions.PloS one · 2015Article
- PRISM offers a comprehensive genomic approach to transcription factor function prediction.Genome research · 2013Article
- Prematurity in mice leads to reduction in nephron number, hypertension, and proteinuria.Translational research : the journal of laboratory and clinical medicine · 2012Article
- Defining and redefining the nephron progenitor population.Pediatric nephrology (Berlin, Germany) · 2011Review
- Osmoregulatory defect in adult mice associated with deficient prenatal expression of six2.American journal of physiology. Regulatory, integrative and comparative physiology · 2011Article
- Dicer regulates the development of nephrogenic and ureteric compartments in the mammalian kidney.Kidney international · 2011Article
- Developmental expression patterns of candidate cofactors for vertebrate six family transcription factors.Developmental dynamics : an official publication of the American Association of Anatomists · 2010Article
- The Renin-Angiotensin System in the Development of Salt-Sensitive Hypertension in Animal Models and Humans.Pharmaceuticals (Basel, Switzerland) · 2010Review
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9 authors at 1 institution in 1 country.
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Abstract
The Br/+ mutant mouse displays decreased embryological expression of the homeobox transcription factor Six2, resulting in hertitable renal hypoplasia. The purpose of this study was to characterize the renal physiological consequences of embryonic haploinsuffiency of Six2 by analyzing renal morphology and function in the adult Br heterozygous mutant. Adult Br/+ kidneys weighed 50% less than those from wild-type mice and displayed glomerulopathy. Stereological analysis of renal glomeruli showed that Br/+ kidneys had an average of 88% fewer glomeruli than +/+ kidneys, whereas individual glomeruli in Br/+ mice maintained an average volume increase of 180% compared with normal nephrons. Immunostaining revealed increased levels of endothelin-1 (ET-1), endothelin receptors A (ET(A)) and B (ET(B)), and Na-K-ATPase were present in the dilated renal tubules of mutant mice. Physiological features of chronic renal failure (CRF) including elevated mean arterial pressure, increased plasma creatinine, and dilute urine excretion were measured in Br/+ mutant mice. Electron microscopy of the Br/+ glomeruli revealed pathological alterations such as hypercellularity, extracellular matrix accumulation, and a thick irregular glomerular basement membrane. These results indicate that adult Br/+ mice suffer from CRF associated with reduced nephron number and renal hypoplasia, as well as glomerulopathy. Defects are associated with embryological deficiencies of Six2, suggesting that proper levels of this protein during nephrogenesis are critical for normal glomerular development and adult renal function.
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