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A Decentralized Ex Vivo Murine Bladder Model with the Detrusor Muscle Removed for Direct Access to the Suburothelium during Bladder Filling
Published on: November 28, 2019
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Excitatory purinergic and cholinergic expression changed in a partial bladder outlet obstruction-induced overactive
Jingyi Huang1, Hongliang Li1, Yao Zhang1
1Guangzhou University of Chinese Medicine, No.232 Outer Ring East Road, Higher Education Mega Center, Guangzhou, Guangdong, China.
Scientific Reports
|October 26, 2023
Summary
Overactive bladder (OAB) in rats is linked to increased bladder muscle and collagen, with higher expression of ChAT and SLC17A9. This suggests OAB pathogenesis involves enhanced excitatory purinergic and cholinergic pathways.
Area of Science:
- Urology
- Pathophysiology
- Molecular Biology
Background:
- Overactive bladder (OAB) is a prevalent condition causing significant social burden, necessitating effective treatments.
- The precise pathogenesis of OAB remains incompletely understood, highlighting the need for further research.
- Current understanding lacks clarity on the molecular mechanisms driving OAB symptoms.
Purpose of the Study:
- To establish a rat model of overactive bladder (OAB) via bladder outlet obstruction (BOO).
- To investigate the urodynamic and molecular changes associated with OAB development in the BOO model.
- To explore the potential role of choline acetyltransferase (ChAT) and SLC17A9 in OAB pathogenesis.
Main Methods:
- Surgical induction of bladder outlet obstruction (BOO) in rats to create an OAB model.
- Urodynamic assessments including urine volume, bladder leak point pressure, maximum voiding pressure, and bladder capacity.
- Histological analysis (H&E, Masson's trichrome) and molecular analysis (qPCR, Western blot) for ChAT and SLC17A9 expression.
Main Results:
- The 4-week BOO model demonstrated significantly increased 12-hour urine volume, bladder leak point pressure, maximum voiding pressure, and non-voiding contractions.
- Detrusor muscle contractility increased significantly in response to electrical and carbachol stimulation in the BOO group.
- Elevated mRNA and protein levels of ChAT and SLC17A9 were observed in the bladders of OAB model rats compared to controls.
Conclusions:
- The study successfully established a rat model of overactive bladder (OAB) 4 weeks post-bladder outlet obstruction (BOO).
- Increased expression of choline acetyltransferase (ChAT) and solute carrier family 17 member 9 (SLC17A9) in the OAB model suggests their involvement in the condition.
- Findings indicate that OAB pathogenesis may be associated with heightened excitatory purinergic and cholinergic signaling pathways.
