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A Single Cell Dissociation Approach for Molecular Analysis of Urinary Bladder in the Mouse Following Spinal Cord Injury
Published on: June 17, 2020
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Molecular Characterization of Non-Neurogenic and Neurogenic Lower Urinary Tract Dysfunction (LUTD) in SCI-Induced and
Michelle von Siebenthal1, Akshay Akshay1,2, Mustafa Besic1
1Functional Urology Research Laboratory, Department for BioMedical Research DBMR, University of Bern, 3008 Bern, Switzerland.
International Journal of Molecular Sciences
|February 11, 2023
Summary
Spinal cord injury (SCI) causes severe bladder dysfunction and fibrosis due to detrusor sphincter dyssynergia. Partial bladder outlet obstruction (pBOO) causes temporary dysfunction but allows bladder compensation, unlike SCI.
Area of Science:
- Urology
- Neuroscience
- Genetics
Background:
- Lower urinary tract dysfunction (LUTD) is a common complication of spinal cord injury (SCI) and bladder outlet obstruction (BOO).
- Understanding the distinct and shared mechanisms underlying neurogenic and obstructive LUTD is crucial for developing targeted therapies.
Purpose of the Study:
- To compare bladder function, gene expression, and morphological changes in mouse models of SCI and partial bladder outlet obstruction (pBOO).
- To elucidate the specific and common features of neurogenic and obstructive LUTD.
Main Methods:
- Repeated urodynamic investigations (UDI) with external urethral sphincter (EUS) electromyography (EMG) in awake restrained mice.
- Histological and transcriptome analysis of bladders post-injury/obstruction.
- Comparative analysis of SCI and pBOO models.
Main Results:
- SCI induced detrusor sphincter dyssynergia (DSD), high-pressure oscillations, inability to void, bladder fibrosis, and significant gene expression changes related to extracellular matrix remodeling and neuronal signaling.
- pBOO caused transiently increased maximal bladder pressure (Pmax) and bladder-to-bodyweight ratio, with gene expression changes involving immune and inflammatory pathways.
- Both SCI and pBOO activated Wnt and TGF-beta signaling; FGF2 was upregulated in both models during bladder remodeling.
Conclusions:
- SCI-induced DSD leads to profound, persistent bladder changes including fibrosis, driven by altered neuronal signaling and muscle contractility.
- pBOO-induced bladder remodeling allows for functional compensation and preservation of normal micturition parameters.
- Comparative analysis highlights distinct pathological pathways and shared molecular responses in neurogenic versus obstructive LUTD.
