Angiotensin Type Ii Receptor Expression and Ureteral Budding

Oshima, Keisuke; Miyazaki, Yoichi; Brock, John W.; Adams, Mark C.; Ichikawa, Iekuni; Pope, John C.

doi:10.1097/00005392-200111000-00066

Cited by 23 publications

(35 citation statements)

References 14 publications

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“…According to the developmental theory of VUR (24), ectopic ureteral budding results in defective vesicoureteral valve, resulting in VUR. Recent findings showed that ectopic budding occurs in angiotensin type II receptor (AT2) null mutant embryos (25). Angiotensin II has also been reported to regulate vascular endothelial growth factor (VEGF) synthesis at the initiation phase of translation of VEGF mRNA in proximal tubular epithelial cells (26).…”

Section: Discussionmentioning

confidence: 99%

Genetic Control of VEGF and TGF-β1 Gene Polymorphisms in Childhood Urinary Tract Infection and Vesicoureteral Reflux

et al. 2007

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ABSTRACT:We investigated whether genetic polymorphisms of vascular endothelial growth factor (VEGF) and transforming growth factor-␤1 (TGF-␤1), potential candidate genes in the pathogenesis of urinary tract infection (UTI) and vesicoureteral reflux (VUR), are associated with the susceptibility to UTI and VUR, and renal scarring. We recruited 89 controls and 86 UTI and 58 VUR children. The UTI group was subdivided into two groups according to renal scarring. Two polymorphisms of VEGF and three of TGF-␤1 genes were investigated by using PCR-restriction fragment length polymorphism analysis. In both UTI and VUR groups, there was an increase in frequency of the VEGF -460 CC (control, 4.3; UTI, 15.9; VUR, 17.8%; p Ͻ 0.05), TGF-␤1 -509 CC (control, 8.7; UTI, 34.6; VUR, 35.1%; p Ͻ 0.001), and TGF-␤1 -800 GG genotypes (control, 19.1; UTI, 40.5; VUR, 40.4%; p Ͻ 0.05). An increase in the TGF-␤1 ϩ869 CC (scar-positive, 35.4; scar-negative, 10.3%; p Ͻ 0.05) and a decrease in the ϩ869 TC genotype (scar-positive, 29.2; scarnegative, 55.2%; p Ͻ 0.05) were observed in the scar-positive subjects. There were no differences in ϩ405 VEGF genotype frequencies. The VEGF T-460C and the TGF-␤1 C-509T, G-800A, and T869C polymorphisms could be genetic markers of the process of UTI and VUR. (Pediatr Res 62: 183-187, 2007)

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Section: Discussionmentioning

confidence: 99%

Genetic Control of VEGF and TGF-β1 Gene Polymorphisms in Childhood Urinary Tract Infection and Vesicoureteral Reflux

et al. 2007

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“…To date, there is no gold standard for measuring the position of the ureteric bud along the mesonephric duct (16,23). Miyazaki et al (19) looked at Bmp4ϩ/Ϫ mice and found a more cranially placed ureteric bud that they scored in relation to the nearest somite.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of RET leads to vesicoureteric reflux in mice

Murawski

Myburgh

et al. 2004

American Journal of Physiology-Renal Physiology

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, a tyrosine kinase receptor essential for kidney development, has recently been shown to be important for the formation of the urinary tract. When RET is overexpressed in the HoxB7/Ret transgenic mouse, kidneys are small and cystic, and in some of the mice, the ureters are grossly dilated. Here, we report that the observed ureteral dilatation is associated with the urinary tract abnormality vesicoureteric reflux (VUR), in which urine flows retrogradely from the bladder to the ureter. Reflux was determined in vitro by injecting methylene blue into the bladders of HoxB7/Ret and wild-type mice. At postnatal day 1, 30% of HoxB7/Ret mice had VUR compared with 4% of wild-type mice (P Ͻ 0.05). The length of the intravesical ureteral tunnel was shorter in HoxB7/Ret mice compared with wild-type mice, on both the right and the left sides (P Ͻ 0.05), suggesting a basis for the higher incidence of VUR in these mutants. At embryonic day 11, the ureteric bud was found to exit more caudally from the mesonephric duct in HoxB7/Ret mice, and this may predispose them to VUR (P Ͻ 0.05). Wild-type and HoxB7/Ret mice were tested for reflux at embryonic day 17, and both showed a high frequency of VUR (59 and 75%, respectively). These results suggest that VUR may occur transiently during normal urinary tract development before the ureter has completed its insertion into the bladder. In the HoxB7/Ret mouse, overexpression of RET appears to delay the maturation of the distal ureter, resulting in postnatal VUR. The HoxB7/Ret mouse is thus an important model in which to examine how vesicoureteric reflux arises during urinary tract development. kidney defect; urinary tract defect; ureteric bud PRIMARY VESICOURETERIC REFLUX (VUR) is a urinary tract abnormality in which urine flows retrogradely from the bladder to the ureters because of an anatomic defect at the junction of the ureter and the bladder. It affects 1-2% of children and predisposes them to recurrent urinary tract infections and in some cases, end-stage renal disease (7, 33). The condition is hereditary: it frequently affects multiple family members, and several genetic loci have been identified from linkage studies of affected families (5, 6).VUR is normally prevented by a functional valve, the flap-valve mechanism, that forms at the site of the ureteral insertion into the bladder. The flap-valve is dependent on 1) the tunnel in which the ureter enters into the bladder, 2) the presence of a muscular layer within the bladder and the ureter, and 3) the position of the ureteral orifice in the muscular layer within the bladder (the trigone). When the bladder is distended with urine, the tunnel is compressed, and this prevents the retrograde passage of urine from the bladder to the kidneys.The length of the intravesical ureteral tunnel is critical for the flap-valve mechanism: shorter tunnels have been identified in patients with VUR (17, 32). Other anatomic findings that have been associated with VUR include a lack of musculature within the ureter and its tunnel (30) and a ureteral ...

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“…45 Studies have shown that induced obstruction in animal fetuses results in renal parenchymal abnormality, but presence of VUR was not determined. 46,47 The second theory proposes that abnormal ureteric budding and/or dysfunctional interactions between the ureteric bud and metanephric mesenchyme give rise to VUR and other renal abnormalities 48. Mouse embryo studies 38,49,50 demonstrate that abnormal ureteric budding was evident in many of the mice that developed renal tract anomalies. Investigators propose that abnormal budding explains the occurrence of VUR.…”

Section: Developmental Aspectsmentioning

confidence: 99%