Segmental up‐regulation of transforming growth factor‐β in the pathogenesis of primary megaureter. An immunocytochemical study

Abstract

Objective To examine the maturational-delay hypothesis were like the fetal ureteric buds at 26-38 weeks of gestation. Positive TGF-b immunoreactions were of primary megaureter (PM), i.e. that the condition arises by a segmental maturational delay of the uretdetected in the longitudinal muscle layer in the ureter from patients 6-12 months old. Such reactions weakeric wall that can resolve spontaneously within the first year of life, using comparative immunocytochemened progressively in those patients older than 1 year, becoming negative in all children older than 3 years. istry of ureters resected from infants and from homologous pre-natal ureters.The TGF-b immunolabelling in resected ureters was closely similar to that in fetal ureters from 20 to Materials and methods Seventeen distal urinary tracts were obtained from children with PM who were 26-week old calves. Conclusions From these results, PM should be ascribed referred for surgery (aged 6 months to 8 years, mean 2.1 years). These were compared with ureteric buds to a segmental developmental delay of the terminal ureter arising at about 20 weeks of gestation, with a obtained from 11-week-old human and 11-to 38-week-old calf fetuses. The samples were immunospossible pathogenetic involvement of autocrine TGF-b overexpression. tained using a monoclonal antibody specific for transforming growth factor b (TGF-b).

Altered ‘active’ antireflux mechanism in primary vesico‐ureteric reflux: a morphological and manometric study

“…Alternatively, as mesenchymal cells, surrounding the mesonephric duct, differentiate into the ureteric inner layer of smooth muscle cells [22], the delayed elongation of the Wolffian duct endings might be a pathogenetic event for muscular and subsequent ICC defects in VUR. Thus, the late maturation of ureteric ends is coherent with a possible spontaneous resolution of VUR, after postnatal remodelling of the VUJ, as shown for the pathogenesis of primary megaureter [23]. Loss of c‐kit‐positive ICCs could be also secondary to ureteric trauma during episodes of VUR, as reported in the proximal segment of obstructed fetal bowel [24].…”

CAVEOLAE ARE NEGATIVE REGULATORS OF TRANSFORMING GROWTH FACTOR-β1 SIGNALING IN URETERAL SMOOTH MUSCLE CELLS

“…5,12 To evaluate the role of TGF-␤1 in the regulation of ureteral smooth muscle we performed mRNA and protein analysis for TGF-␤1, types I and II TGF-␤ receptors, and the signaling mediator Smad-2 in USMCs. TGF-␤1 mRNA was detected in exponentially growing cultures of SMC (0 hours of serum depletion) ( fig.…”

“…These observations are consistent with the fibrosis inducing activity of TGF-␤1 identified in many disease conditions. In contrast, increased TGF-␤1 expression has been linked to smooth muscle hypoplasia in conditions such as megaureter, 5 suggesting that the growth regulating activities of TGF-␤1 are context dependent.…”

“…In the urinary tract TGF-␤1 has been implicated in renal and ureteropelvic junction fibrosis in response to obstruction 4 and it has also been linked to the distal ureteral smooth muscle (SM) hypoplasia observed in primary obstruction megaureter. 5 However, to our knowledge the effects of TGF-␤1 on isolated ureteral SM cells (USMCs) have not been described.…”

Physiopathology of vesico-ureteral reflux

“…Conversely, as mesenchymal cells, sorround the mesonephric duct, differentiate into the ureteric inner layer of smooth muscle cells [21], the delayed elongation of the Wolffian duct endings might be a pathogenetic event for muscular and subsequent ICC defects in VUR. Thus, the delayed maturation of ureteric ends is coherent with a possible spontaneous resolution of VUR, after postnatal remodelling of the VUJ, as shown for the pathogenesis of primary megaureter [22]. …”