ArticleThe Journal of biological chemistry2015
Trpm7 Protein Contributes to Intercellular Junction Formation in Mouse Urothelium.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Ion Channels as Therapeutic Targets in Overactive Bladder: A Narrative Review of Mechanisms, Translational Evidence, and Current Gaps.Lower urinary tract symptoms · 2026Review
- Review
- The TRPM8 channel as a potential therapeutic target for bladder hypersensitive disorders.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022Review
- What is the Cause of Recurrent Urinary Tract Infection? Contemporary Microscopic Concepts of Pathophysiology.International neurourology journal · 2021Article
- Transient receptor potential channels in sensory mechanisms of the lower urinary tract.Nature reviews. Urology · 2021Review
- The Urothelium: Life in a Liquid Environment.Physiological reviews · 2020Review
- A non-enzymatic method for dissection of mouse bladder urothelial tissue.Nature protocols · 2019Article
- Role of TRPM7 in Cancer: Potential as Molecular Biomarker and Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2017Review
- Roles of transient receptor potential channels in regulation of vascular and epithelial barriers.Tissue barriers · 2017Article
- Expression of the TRPM6 in mouse placental trophoblasts; potential role in maternal-fetal calcium transport.The journal of physiological sciences : JPS · 2017Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trpm7 is a divalent cation-permeable channel that has been reported to be involved in magnesium homeostasis as well as cellular adhesion and migration. We generated urothelium-specific Trpm7 knock-out (KO) mice to reveal the function of Trpm7 in vivo. A Trpm7 KO was induced by tamoxifen and was confirmed by genomic PCR and immunohistochemistry. By using patch clamp recordings in primary urothelial cells, we observed that Mg(2+)-inhibitable cation currents as well as acid-inducible currents were significantly smaller in Trpm7 KO urothelial cells than in cells from control mice. Assessment of voiding behavior indicated a significantly smaller voided volume in Trpm7 KO mice (mean voided volume 0.28 ± 0.08 g in KO mice and 0.36 ± 0.04 g in control mice, p < 0.05, n = 6-8). Histological analysis showed partial but substantial edema in the submucosal layer of Trpm7 KO mice, most likely due to inflammation. The expression of proinflammatory cytokines TNF-α and IL-1β was significantly higher in Trpm7 KO bladders than in controls. In transmission electron microscopic analysis, immature intercellular junctions were observed in Trpm7 KO urothelium but not in control mice. These results suggest that Trpm7 is involved in the formation of intercellular junctions in mouse urothelium. Immature intercellular junctions in Trpm7 knock-out mice might lead to a disruption of barrier function resulting in inflammation and hypersensitive bladder afferent nerves that may affect voiding behavior in vivo.
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