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Related Experiment Video

Updated: Jun 20, 2026

Expression of Transgenes in Native Bladder Urothelium Using Adenovirus-Mediated Transduction
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Expression of Transgenes in Native Bladder Urothelium Using Adenovirus-Mediated Transduction

Published on: October 6, 2022

Prolonged peritoneal gene expression using a helper-dependent adenovirus.

Limin Liu1, Chang-Xin Shi, Ayesha Ghayur

  • 1Department of Medicine, McMaster University, Hamilton, Ontario, Canada.

Peritoneal Dialysis International : Journal of the International Society for Peritoneal Dialysis
|September 25, 2009
PubMed
Summary

A novel helper-dependent adenovirus model in mice successfully replicated encapsulating peritoneal sclerosis (EPS) by prolonging transforming growth factor-beta 1 (TGF-beta1) expression, aiding EPS research.

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Area of Science:

  • Biomedical Research
  • Animal Models
  • Gastroenterology

Background:

  • Encapsulating peritoneal sclerosis (EPS) is a rare, multifactorial complication of peritoneal dialysis.
  • The exact causes of EPS remain poorly understood.
  • A robust animal model is crucial for studying EPS pathophysiology and developing treatments.

Purpose of the Study:

  • To develop and validate a novel animal model for encapsulating peritoneal sclerosis (EPS).
  • To investigate the role of prolonged transforming growth factor-beta 1 (TGF-beta1) expression in EPS development.
  • To establish a platform for evaluating potential therapeutic interventions for EPS.

Main Methods:

  • A helper-dependent adenovirus (HDAdTGF-beta1) expressing TGF-beta1 and GFP was engineered.

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Last Updated: Jun 20, 2026

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  • Mice received intraperitoneal injections of HDAdTGF-beta1, first-generation AdTGF-beta1, or control AdGFP.
  • Peritoneal response, transgene expression duration, and histological changes were monitored.
  • Main Results:

    • HDAdTGF-beta1 induced sustained transgene expression (over 74 days) compared to transient expression (<28 days) with first-generation adenovirus.
    • HDAdTGF-beta1 treatment resulted in progressive peritoneal fibrosis, adhesion formation, and bowel encapsulation.
    • Mice treated with HDAdTGF-beta1 showed significantly reduced weight gain and minimal inflammation.

    Conclusions:

    • Prolonged TGF-beta1 expression via HDAdTGF-beta1 effectively models the peritoneal morphology of EPS.
    • Transient TGF-beta1 expression led to a resolving fibrotic response, mimicking simple peritoneal sclerosis.
    • This novel HDAdTGF-beta1 model provides a valuable tool for understanding EPS mechanisms and testing treatments.