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Knockdown of FKBP12.6 may Cause Bladder Dysfunction in Mice by Affecting IP3R/TRPM4 Function
Jiang Zhao1, Hao Zhou2, Jun Wang3
1Department of Urology, Second Affiliated Hospital, Army Medical University, Chongqing, 400037, China.
Current Medicinal Chemistry
|March 7, 2025
Summary
FKBP12.6 (FK506 binding protein 12.6) deficiency leads to bladder dysfunction by altering IP3R/TRPM4 channel activity. Reduced FKBP12.6 expression in obstructed bladders exacerbates urinary issues.
Area of Science:
- Urology
- Molecular Biology
- Physiology
Background:
- FKBP12.6 is a key regulator of bladder excitatory contraction.
- Its role in bladder dysfunction, particularly in response to obstruction, requires further investigation.
Purpose of the Study:
- To investigate the impact of FKBP12.6 deficiency on bladder function.
- To explore the relationship between FKBP12.6, IP3R, and TRPM4 in bladder contraction.
Main Methods:
- Utilized FKBP12.6 knockout mice and a Partial Bladder Outlet Obstruction (PBOO) model.
- Assessed bladder function via void spot assays, urodynamic tests, and visceromotor response.
- Examined protein expression and interactions using Western blot and co-immunoprecipitation.
Main Results:
- FKBP12.6 expression decreased in PBOO mice.
- FKBP12.6 knockout mice exhibited increased micturition frequency, bladder sensitivity, and detrusor instability.
- FKBP12.6 directly binds to IP3R, influencing IP3R/TRPM4 pathway activity and bladder sensitivity.
Conclusions:
- FKBP12.6 downregulation in PBOO mice contributes to bladder dysfunction.
- FKBP12.6 deletion impairs bladder function by affecting IP3R/TRPM4 channel activity.
