Association between congenital defects in papillary outgrowth and functional obstruction in Crim1 mutant mice

@article{Wilkinson2012AssociationBC,
  title={Association between congenital defects in papillary outgrowth and functional obstruction in Crim1 mutant mice},
  author={Lorine Wilkinson and Nyoman D. Kurniawan and Yu Leng Phua and Michael J. Nguyen and Joan Li and Graham J. Galloway and Hikaru Hashitani and Richard J. Lang and Melissa Helen Little},
  journal={The Journal of Pathology},
  year={2012},
  volume={227},
  url={https://api.semanticscholar.org/CorpusID:2777257}
}
Results highlight the previously unrecognized association between defects in papillary development and progression to chronic kidney disease later in life, as well as implicating Crim1 in Papillary extension and pelvic smooth muscle contractility.
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10 Citations
Background Citations
4
Methods Citations
2

10 Citations

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41 References

Loss of renal microvascular integrity in postnatal Crim1 hypomorphic transgenic mice.

This study suggests that Crim1 is involved in endothelial maintenance and integrity and its loss contributes to a primary defect in the extraglomerular vasculature.

Crim1KST264/KST264 mice implicate Crim1 in the regulation of vascular endothelial growth factor-A activity during glomerular vascular development.

This is the first in vivo demonstration of regulation of VEGF-A delivery and supports the hypothesis that Crim1 functions to regulate the release of growth factors from the cell of synthesis.

Crim1KST264/KST264 mice display a disruption of the Crim1 gene resulting in perinatal lethality with defects in multiple organ systems

The severe and complex phenotype observed in Crim1KST264/K ST264 mice highlights the importance of Crim1 in numerous aspects of organogenesis.

Calcineurin is required in urinary tract mesenchyme for the development of the pyeloureteral peristaltic machinery.

It is demonstrated that calcineurin is an essential signaling molecule in urinary tract development and is required for normal proliferation of the urinary tract mesenchymal cells in a cell-autonomous manner.

GLI3 repressor controls functional development of the mouse ureter.

It is determined that Hh signaling controls 2 cell populations required for the initiation and transmission of coordinated ureter contractions, and genetic inactivation of Gli3 in Smo-deficient mice rescued their hydronephrosis, hydroureter, Kit and Hcn3 expression, and Ureter peristalsis.

Antagonism of BMP4 signaling disrupts smooth muscle investment of the ureter and ureteropelvic junction.

Renin–angiotensin system in ureteric bud branching morphogenesis: insights into the mechanisms

The role of the RAS is described in UB branching morphogenesis and emerging insights into the cellular and molecular mechanisms whereby RAS regulates this critical morphogenetic process are highlighted.

Renal structural and functional repair in a mouse model of reversal of ureteral obstruction.

The regenerative potential of the kidney after the established interstitial matrix expansion and medullary ablation associated with UUO in the adult mouse is described.

Ureteral obstruction as a model of renal interstitial fibrosis and obstructive nephropathy.

The UUO model is likely to reveal useful biomarkers of progression of renal disease, as well as new therapies, which are desperately needed to allow intervention before the establishment of irreversible renal injury.

Embryology and genetics of primary vesico-ureteric reflux and associated renal dysplasia

An overview of the embryology and genetics of primary VUR and associated congenital reflux nephropathy is presented, supporting the hypothesis that VUR is genetically heterogeneous and is caused by a number of different genes acting with random environmental effects.