ArticleInternational journal of molecular sciences2023
Myostatin Overexpression and Smad Pathway in Detrusor Derived from Pediatric Patients with End-Stage Lower Urinary Tract Dysfunction.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 2 citations in OpenAlex.
- LEM-Domain-Containing Inner Nuclear Membrane Proteins: Emerging Regulators of Intranuclear Signaling.International journal of molecular sciences · 2026Review
- Extracellular vesicles in cancer-associated cachexia: molecular mechanisms and therapeutic perspectives.Frontiers in cell and developmental biology · 2026Review
- Low-Intensity Extracorporeal Shock Wave Therapy Alleviates Detrusor Muscle Apoptosis and Extracellular Matrix Dysregulation in the Bladder of Diabetic Rats.International journal of medical sciences · 2026Article
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Authors and funding
5 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Cell therapies and tissue engineering approaches using smooth muscle cells (SMCs) may provide treatment alternatives for end-stage lower urinary tract dysfunction (ESLUTD). Myostatin, a negative regulator of muscle mass, is a promising target to improve muscle function through tissue engineering. The ultimate goal of our project was to investigate the expression of myostatin and its potential impact in SMCs derived from healthy pediatric bladders and pediatric ESLUTD patients. Human bladder tissue samples were evaluated histologically, and SMCs were isolated and characterized. The proliferation of SMCs was assessed by WST-1 assay. The expression pattern of myostatin, its pathway and the contractile phenotype of the cells were investigated at gene and protein levels by real-time PCR, flow cytometry, immunofluorescence, WES and gel contraction assay. Our results show that myostatin is expressed in human bladder smooth muscle tissue and in isolated SMCs at gene and protein levels. A higher expression of myostatin was detected in ESLUTD-derived compared to control SMCs. Histological assessment of bladder tissue confirmed structural changes and decreased muscle-to-collagen ratios in ESLUTD bladders. A decrease in cell proliferation and in the expression of key contractile genes and proteins, α-SMA, calponin, smoothelin and MyH11, as well as a lower degree of in vitro contractility was observed in ESLUTD-derived compared to control SMCs. A reduction in the myostatin-related proteins Smad 2 and follistatin, and an upregulation in the proteins p-Smad 2 and Smad 7 were observed in ESLUTD SMC samples. This is the first demonstration of myostatin expression in bladder tissue and cells. The increased expression of myostatin and the changes in the Smad pathways were observed in ESLUTD patients. Therefore, myostatin inhibitors could be considered for the enhancement of SMCs for tissue engineering applications and as a therapeutic option for patients with ESLUTD and other smooth muscle disorders.
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