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Related Experiment Video

Updated: Jun 15, 2026

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

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

Published on: April 27, 2014

MIF-Modulated Spinal Proteins Associated with Persistent Bladder Pain: A Proteomics Study.

Shaojing Ye¹, Nilesh M Agalave², Fei Ma¹

¹Research & Development, Lexington VA Health Care System, Lexington, KY 40502, USA.

International Journal of Molecular Sciences

|April 27, 2024

Summary

This summary is machine-generated.

Spinal macrophage migration inhibitory factor (MIF) and its receptors drive persistent bladder pain in mice. Targeting these pathways may offer new treatments for bladder pain conditions like Interstitial Cystitis/Bladder Pain Syndrome.

Keywords:

CD74 CXCR4 macrophage migration inhibitory factor persistent bladder pain spinal proteins

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Area of Science:

Neuroscience
Immunology
Pain Research

Background:

Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS) is characterized by bladder pain.
Spinal mechanisms, particularly involving macrophage migration inhibitory factor (MIF), are implicated in persistent bladder hyperalgesia (BHA).

Purpose of the Study:

To investigate the role of spinal MIF receptors in mediating persistent BHA.
To identify spinal proteomic changes associated with BHA and its relief via MIF antagonism.

Main Methods:

Induction of persistent BHA in mice using intravesical Protease Activated Receptor-4 (PAR4) activation.
Administration of intrathecal MIF monoclonal antibodies (mAb) or isotype control.
Antagonism of MIF receptors (CD74, CXCR4).
Spinal proteomics analysis (LC-MS/MS) of L6-S1 segments.

Main Results:

Intrathecal MIF antagonism temporarily reversed persistent BHA.
Antagonism of MIF receptors CD74 and CXCR4 partially reversed BHA.
Proteomics identified significant changes in specific spinal proteins during BHA, which were reversed by MIF antagonism.

Conclusions:

Spinal MIF and its receptors (CD74, CXCR4) are key mediators of persistent bladder pain.
MIF-modulated spinal proteins represent potential therapeutic targets for BHA and IC/BPS.