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Published on: August 13, 2020
Social stress in mice induces voiding dysfunction and bladder wall remodeling.
Andy Chang1, Stephan Butler, Joanna Sliwoski
1Division of Urology, The Children's Hospital of Philadelphia, Philadelphia, PA 19104, USA.
American Journal of Physiology. Renal Physiology
|July 10, 2009
Summary
Social stress in mice caused urinary retention and increased bladder mass. Molecular changes in transcription factors and DNA synthesis contribute to bladder wall remodeling, offering insights into human dysfunctional voiding.
Area of Science:
- Urology
- Neuroscience
- Molecular Biology
Background:
- Social stress is anecdotally linked to altered urinary voiding patterns in rodents.
- Previous research characterized urodynamic and central changes in a rat model of social defeat.
Purpose of the Study:
- To characterize social stress-induced voiding phenotype in mice.
- To investigate molecular mechanisms underlying bladder wall remodeling due to social stress.
- To explore the relevance to human dysfunctional voiding with psychological components.
Main Methods:
- FVB mice were subjected to a 4-week social stress paradigm or control manipulation.
- In vivo cystometry was performed to assess urodynamic parameters.
- Bladder tissue was analyzed for nuclear expression of MEF-2 and NFAT, myosin heavy chain B isoform mRNA, and BrdU uptake.
Main Results:
- Social stress induced altered urinary voiding patterns, suggesting urinary retention and increased bladder mass.
- Cystometry showed an increased volume at micturition without changes in voiding pressure.
- Increased nuclear expression of MEF-2 and NFAT, elevated myosin heavy chain B isoform mRNA, and increased BrdU uptake were observed in stressed bladders.
Conclusions:
- Social stress leads to urinary retention and subsequent bladder wall remodeling.
- Molecular mechanisms involve shifts in transcription factors, myosin heavy chain isoform expression, and increased DNA synthesis.
- This rodent model provides insights into the mechanisms and potential treatments for human dysfunctional voiding.

