ArticlePloS one2021
Intravesical CD74 and CXCR4, macrophage migration inhibitory factor (MIF) receptors, mediate bladder pain.
Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- HLA-DQB1-mediated B cell-epithelial crosstalk drives EBV-associated inflammation in Hunner-type interstitial cystitis.Molecular therapy. Nucleic acids · 2025Article
- Large-Scale Plasma Proteomics to Profile Pathways and Prognosis of Chronic Pain.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Integration of bulk RNA-seq and scRNA-seq reveals transcriptomic signatures associated with deep vein thrombosis.Frontiers in genetics · 2025Article
- Mechanisms of oxidative stress in interstitial cystitis/bladder pain syndrome.Nature reviews. Urology · 2024Review
- MIF-Modulated Spinal Proteins Associated with Persistent Bladder Pain: A Proteomics Study.International journal of molecular sciences · 2024Article
- Lumbosacral spinal proteomic changes during PAR4-induced persistent bladder pain.Neuroscience letters · 2024Article
- Article
- Bladder Oxidative Stress and HMGB1 Release Contribute to PAR4-Mediated Bladder Pain in Mice.Frontiers in systems neuroscience · 2022Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundActivation of intravesical protease activated receptor 4 (PAR4) leads to release of urothelial macrophage migration inhibitory factor (MIF). MIF then binds to urothelial MIF receptors to release urothelial high mobility group box-1 (HMGB1) and elicit bladder hyperalgesia. Since MIF binds to multiple receptors, we investigated the contribution of individual urothelial MIF receptors to PAR4-induced HMGB1 release in vivo and in vitro and bladder pain in vivo. METHODOLOGY/PRINCIPAL
findingsWe tested the effect of intravesical pre-treatment with individual MIF or MIF receptor (CD74, CXCR4, CXCR2) antagonists on PAR4-induced HMGB1 release in vivo (female C57/BL6 mice) and in vitro (primary human urothelial cells) and on PAR4-induced bladder hyperalgesia in vivo (mice). In mice, PAR4 induced HMGB1 release and bladder hyperalgesia through activation of intravesical MIF receptors, CD74 and CXCR4. CXCR2 was not involved in these effects. In primary urothelial cells, PAR4-induced HMGB1 release through activation of CD74 receptors. Micturition parameters in mice were not changed by any of the treatments. CONCLUSIONS/SIGNIFICANCE: Urothelial MIF receptors CD74 and CXCR4 mediate bladder pain through release of urothelial HMGB1. This mechanism may set up persistent pain loops in the bladder and warrants further investigation. Urothelial CD74 and CXCR4 may provide novel targets for interrupting bladder pain.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.