ArticleScientific reports2022
Human amniotic fluid stem cells can alleviate detrusor dysfunction caused by bladder outlet obstruction in rats.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 4 citations in OpenAlex.
- Mesenchymal stem Cells and Extracellular Vesicles in Bladder Dysfunction: Mechanisms and Translational Perspectives.Stem cell reviews and reports · 2026Review
- Human Amniotic Fluid Stem Cell-mediated Biomechanical Restoration of Urinary Continence in Rats.Tissue engineering and regenerative medicine · 2026Article
- Stem Cell-Based Strategies for Fibrotic and Neurogenic Bladder Disorders: Current Evidence, Translational Challenges, and Future Directions.Current issues in molecular biology · 2026Review
- Extracellular vesicles derived from human amniotic fluid stem cells improve bladder dysfunction in rat model of diabetic atherosclerosis.World journal of stem cells · 2026Article
- Bladder dysfunction in hypoestrogenic rats with metabolic syndrome can be ameliorated after amniotic fluid stem cell treatment.Stem cells translational medicine · 2025Article
- Local Injection of Stem Cells Can Be a Potential Strategy to Improve Bladder Dysfunction after Outlet Obstruction in Rats.International journal of molecular sciences · 2024Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study examined whether bladder detrusor dysfunction due to partial bladder outlet obstruction (pBOO) could be improved after the treatment of human amniotic fluid stem cells (hAFSCs). 72 female rats were grouped into sham operation, pBOO, and pBOO with hAFSCs treatment (pBOO + hAFSCs) for in vitro and in vivo studies. Bladder weight, bladder wall thickness, the ratio of collagen to smooth muscle and the levels of positive CD11b/c and HIS48 cells was significantly increased after pBOO but improved after hAFSCs treatment. Cystometries showed impaired bladder function after pBOO. Protein and mRNA levels of hypoxia inducible factor-1α, CCL2, interleukin-1β, transforming growth factor-β1 (TGF-β1), connective tissue growth factor (CTGF), α-smooth muscle actin, collagen I and collagen III were increased at 2 and/or 6 weeks, but proteins and mRNA expressions of protein gene product 9.5 were decreased at 2 and 6 weeks after pBOO. These abnormalities were improved after hAFSCs treatment. The expressions of TGF-β1 and CTGF in cultured detrusor cells of pBOO rats were increased but were improved after hAFSCs treatment. The present results showed hAFSCs treatment could improve bladder detrusor dysfunction in pBOO rats, which may be related to the reduction of inflammatory and pro-fibrotic markers in detrusor muscle cells.
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