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Local Injection of Stem Cells Can Be a Potential Strategy to Improve Bladder Dysfunction after Outlet Obstruction in Rats. | LitMetric

AI Article Synopsis

  • This study explores the effects of human amniotic fluid stem cells (hAFSCs) on bladder function in rats with partial bladder outlet obstruction (pBOO).
  • Thirty-six female rats were tested, with some receiving hAFSC injections and others not, while several cellular factors related to bladder function and health were measured over two different time periods.
  • The findings indicate that hAFSCs can improve bladder dysfunction by inhibiting certain signaling pathways and reducing collagen buildup, suggesting potential therapeutic benefits for patients with bladder outlet obstruction.

Article Abstract

This study investigates whether hAFSCs can improve bladder function in partial bladder outlet obstruction (pBOO) rats by targeting specific cellular pathways. Thirty-six female rats were divided into sham and pBOO groups with and without hAFSCs single injection into the bladder wall. Cystometry, inflammation/hypoxia, collagen/fibrosis/gap junction proteins, and smooth muscle myosin/muscarinic receptors were examined at 2 and 6 weeks after pBOO or sham operation. In pBOO bladders, significant increases in peak voiding pressure and residual volume stimulated a significant upregulation of inflammatory and hypoxic factors, TGF-β1 and Smad2/3. Collagen deposition proteins, collagen 1 and 3, were significantly increased, but bladder fibrosis markers, caveolin 1 and 3, were significantly decreased. Gap junction intercellular communication protein, connexin 43, was significantly increased, but the number of caveolae was significantly decreased. Markers for the smooth muscle phenotype, myosin heavy chain 11 and guanylate-dependent protein kinase, as well as M2 muscarinic receptors, were significantly increased in cultured detrusor cells. However, hAFSCs treatment could significantly ameliorate bladder dysfunction by inactivating the TGFβ-Smad signaling pathway, reducing collagen deposition, disrupting gap junctional intercellular communication, and modifying the expressions of smooth muscle myosin and caveolae/caveolin proteins. The results support the potential value of hAFSCs-based treatment of bladder dysfunction in BOO patients.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11313184PMC
http://dx.doi.org/10.3390/ijms25158310DOI Listing

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