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Chronic cyclic bladder over distention up-regulates hypoxia dependent pathways.

Heidi A Stephany¹, Douglas W Strand, Christina B Ching

¹Division of Pediatric Urology, Monroe Carell Jr. Children's Hospital at Vanderbilt, Nashville, Tennessee.

The Journal of Urology

|February 23, 2013

Summary

Chronic bladder distention in mice causes tissue hypoxia and inflammation, leading to an overactive voiding pattern. This model helps understand bladder dysfunction in patients with poor bladder emptying.

Keywords:

Arnt2 Ctgf F2-IsoP F2-isoprostane Glut-1 Gpx1 HIF Hmox1 ROS anoxia arylhydrocarbon receptor nuclear translocator 2 connective tissue growth factor gene expression glucose transporter 1 glutathione peroxidase 1 hemoxygenase 1 hypoxia-inducible factor oxidative stress pBOO partial bladder outlet obstruction qRT-PCR quantitative real-time polymerase chain reaction reactive oxygen species urinary bladder urinary bladder neck obstruction

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Area of Science:

Urology
Pathology
Physiology

Background:

Bladder overdistention can cause decreased elasticity and contractile dysfunction.
Hypoxia-dependent signaling pathways may be activated by chronic bladder distention.

Purpose of the Study:

To investigate if chronic bladder distention in a murine model activates hypoxia-dependent signaling pathways.
To characterize the pathological and functional changes in the bladder following chronic distention.

Main Methods:

Female mice underwent urethral catheterization and bladder distention.
Bladder tissue was analyzed using histology, immunohistochemistry for hypoxia markers (Glut-1, Hypoxyprobe™-1), and gene expression analysis (real-time PCR).
Oxidative stress and functional bladder changes (voiding patterns) were assessed.

Main Results:

Distention induced inflammatory changes and tissue hypoxia.
Hypoxia and oxidative stress-related genes (Hif1a, Arnt2, Ctgf, Gpx1, Hmox1) were upregulated.
Voided urine blots showed an overactive voiding pattern after distention.

Conclusions:

Chronic bladder distention is feasible in female mice, causing hypoxic injury.
The observed functional changes include increased voiding patterns.
This model may replicate bladder dysfunction in patients with poor bladder emptying, such as those with neurological disease.