ArticleThe Journal of clinical investigation2011
GLI3 repressor controls functional development of the mouse ureter.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 90 citations in OpenAlex.
- Hedgehog pathway disruption alters urothelial differentiation and continence mechanisms in the female mouse lower urinary tract.American journal of physiology. Renal physiology · 2026Article
- Transcription factor ZEB2 is essential for ureteral smooth muscle cell differentiation.PLoS genetics · 2026Article
- The kidney stroma in development and disease.Nature reviews. Nephrology · 2025Review
- Ureter development and associated congenital anomalies.Nature reviews. Nephrology · 2025Review
- Effect of retention time on renal function and kidney size in patients with indwelling DJ tubes.Scientific reports · 2025Article
- Rab35 Is Required for Embryonic Development and Kidney and Ureter Homeostasis through Regulation of Epithelial Cell Junctions.Journal of the American Society of Nephrology : JASN · 2024Article
- Hedgehog signaling is required for the maintenance of mesenchymal nephron progenitors.bioRxiv : the preprint server for biology · 2024Article
- Ahnak is required to balance calcium ion homeostasis and smooth muscle development in the urinary system.Cell & bioscience · 2023Article
- An evolutionarily conserved pacemaker role for HCN ion channels in smooth muscle.The Journal of physiology · 2023Article
- Hedgehog-GLI mediated control of renal formation and malformation.Frontiers in nephrology · 2023Review
- A Critical Function for the Transcription Factors GLI1 and GLI2 in the Proliferation and Survival of Human Mast Cells.Frontiers in immunology · 2022Article
- Nephronophthisis-Pathobiology and Molecular Pathogenesis of a Rare Kidney Genetic Disease.Genes · 2021Review
- Mediators of human ureteral smooth muscle contraction-a role for erythropoietin, tamsulosin and Gli effectors.Translational andrology and urology · 2021Article
- Hedgehog Signaling: Implications in Cancers and Viral Infections.International journal of molecular sciences · 2021Review
- Roles for urothelium in normal and aberrant urinary tract development.Nature reviews. Urology · 2020Review
- Identification and classification of interstitial cells in the mouse renal pelvis.The Journal of physiology · 2020Article
- Lineage-specific roles of hedgehog-GLI signaling during mammalian kidney development.Pediatric nephrology (Berlin, Germany) · 2020Review
- Hedgehog signalling pathway activation in gastrointestinal stromal tumours is mediated by primary cilia.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2020Article
- Overactivity or blockade of transforming growth factor-β each generate a specific ureter malformation.The Journal of pathology · 2019Article
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5 authors at 3 institutions in 3 countries.
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Abstract
Obstructive and nonobstructive forms of hydronephrosis (increased diameter of the renal pelvis and calyces) and hydroureter (dilatation of the ureter) are the most frequently detected antenatal abnormalities, yet the underlying molecular mechanisms are largely undefined. Hedgehog (Hh) proteins control tissue patterning and cell differentiation by promoting GLI-dependent transcriptional activation and by inhibiting the processing of GLI3 to a transcriptional repressor. Genetic mutations that generate a truncated GLI3 protein similar in size to the repressor in humans with Pallister-Hall syndrome (PHS; a disorder whose characteristics include renal abnormalities) and hydroureter implicate Hh-dependent signaling in ureter morphogenesis and function. Here, we determined that Hh signaling controls 2 cell populations required for the initiation and transmission of coordinated ureter contractions. Tissue-specific inactivation of the Hh cell surface effector Smoothened (Smo) in the renal pelvic and upper ureteric mesenchyme resulted in nonobstructive hydronephrosis and hydroureter characterized by ureter dyskinesia. Mutant mice had reduced expression of markers of cell populations implicated in the coordination of unidirectional ureter peristalsis (specifically, Kit and hyperpolarization-activation cation-3 channel [Hcn3]), but exhibited normal epithelial and smooth muscle cell differentiation. Kit deficiency in a mouse model of PHS suggested a pathogenic role for GLI3 repressor in Smo-deficient embryos; indeed, genetic inactivation of Gli3 in Smo-deficient mice rescued their hydronephrosis, hydroureter, Kit and Hcn3 expression, and ureter peristalsis. Together, these data demonstrate that Hh signaling controls Kit and Hcn3 expression and ureter peristalsis.
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