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Multiple Sclerosis l: Introduction

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Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...

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Urinary Bladder Distention Evoked Visceromotor Responses as a Model for Bladder Pain in Mice

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Pannexin 1 involvement in bladder dysfunction in a multiple sclerosis model.

Hiromitsu Negoro¹, Sarah E Lutz, Louis S Liou

¹Department of Urology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.

Scientific Reports

|July 6, 2013

Summary

This summary is machine-generated.

Multiple Sclerosis (MS) bladder dysfunction involves pannexin 1 (Panx1) signaling. Panx1 depletion in a mouse model reduced bladder dysfunction and inflammation, suggesting Panx1 as a therapeutic target.

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Area of Science:

Neuroimmunology
Urology
Cellular Signaling

Background:

Bladder dysfunction is a frequent complication of Multiple Sclerosis (MS), yet its underlying pathophysiology remains poorly understood.
Key signaling molecules, including pannexin 1 (Panx1) and connexin43 (Cx43), are implicated in bladder function and inflammation.

Purpose of the Study:

To investigate the role of Panx1 in the development of bladder dysfunction in a mouse model of MS.
To elucidate the signaling pathways involving Panx1, Cx43, and inflammatory mediators in the MS bladder.

Main Methods:

Utilized experimental autoimmune encephalomyelitis (EAE), an MS model, in wild-type and Panx1-deficient mice.
Assessed micturition function and analyzed gene expression in bladder tissues.
Investigated the effects of IL-1β stimulation and Panx1 inhibition on urothelial cells in vitro.

Main Results:

EAE mice exhibited micturition dysfunction and altered expression of mechanosensory and signaling genes, including Panx1 and Cx43.
Panx1-deficient EAE mice showed reduced bladder dysfunction compared to wild-type EAE mice, despite similar neurological deficits.
IL-1β stimulation of urothelial cells increased Cx43 expression and inflammatory markers, effects modulated by Panx1 signaling.

Conclusions:

Pannexin 1 signaling contributes to bladder dysfunction in MS by promoting inflammatory responses.
The Panx1-mediated positive feedback loop involving IL-1β and Cx43 represents a potential therapeutic target for MS-related bladder issues.