Quantification of the TGF- <mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" display="inline" id="d1e208" altimg="si6.svg"><mml:mi mathvariant="normal">β</mml:mi></mml:math>/SMAD fibrosis pathway in bladder wall samples from children with congenital lower urinary tract anomalies

Replacement of detrusor smooth muscle (SM) with connective tissue (CT) in the bladder wall has functional consequences to lower urinary tract function, namely changes filling compliance and its contractile performance. In children congenital anomalies such remodelling may underlie poor prognosis that is characteristic a significant proportion these patients. We have quantified extent CT deposition samples from four age-matched (24–72 months) patient groups, namely: normally-functioning (control) bladders; exstrophy, neurogenic bladders (NGB) posterior urethral valves (PUV). addition, using multiplex labelling we also quantified, neighbouring sections, expression TGF-β, downstream transcription factor SMAD2, connexin-43, as well DAPI nuclear material, separately SM regions layer. TGF-β receptor (TGF-βR) Cx43 were greater exstrophy NGB (but not PUV) tissues when compared control, but unchanged regions. SMAD2 was similar all groups both regions, minor increases PUV small reductions staining less between groups. Overall, pathway shows variability anomalies, control tissue, at this period post-natal development extant Antifibrotic strategies target offer an approach minimise fibrotic development.