Level D· Scientific groundwork from lab and animal studiesLaboratory StudyPubMedOpen access

Longitudinal Pilot Study of Progressive Urethral Sub-Obstruction in a Canine Model: Bladder Functional and Structural Changes and Exploratory Evaluation of Autologous Mesenchymal Stem Cells.

Porato M., Noël S., Antoine N., Bolen G., Pincemail J., Garigliany MM.

Laboratory Study on Systemic / IV, published in Vet Sci (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Vet Sci (2026)
Country
Switzerland
Reported sample size
—
Source database
PubMed
PMID
42188930
PMCID
PMC13211550
DOI
10.3390/vetsci13050460

Abstract (original English)

Bladder outlet obstruction (BOO) may lead to detrusor decompensation through progressive bladder remodeling. Most experimental studies rely on acutely induced BOO in rodents. Since progressive obstruction better reflects the condition, non-lethal models are needed to investigate chronic obstruction pathophysiology and evaluate regenerative therapies. This exploratory study aimed to evaluate (1) a progressive BOO model induced by an artificial urethral sphincter (AUS) in 2 dogs and (2) the systemic administration of autologous adipose-derived mesenchymal stem cells (ADMSCs) after obstruction release. Two intact male dogs underwent progressive BOO through gradual AUS inflation. Longitudinal assessment included telemetric urodynamic monitoring, urethral pressure profilometry, ultrasonography, post-void residual measurement, oxidative stress markers in serial blood samples and serial bladder biopsies for histology, transmission electron microscopy, immunohistochemistry, RT-qPCR and RNA sequencing (CCL2, CCR2, GFAP, VEGF, HGF). After AUS removal, one dog received three intravenous injections of 20 × 10 6 PKH26-labelled autologous ADMSCs. BOO induced functional changes (increased detrusor pressure and urethral resistance, decreased urinary flow, prolonged voiding). No detrusor decompensation or fibrosis comparable to the human condition developed, encouraging refinement of this model

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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