ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Loss of β1-integrin from urothelium results in overactive bladder and incontinence in mice: a mechanosensory rather than structural phenotype.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Genetic variants and expression changes in urgency urinary incontinence: A systematic review.Neurourology and urodynamics · 2020Pooled it
- Biomechanical regulation of bladder injury and repair.Nature reviews. Urology · 2026Review
- Amyloid Precursor Protein Processing Links Female Urgency Urinary Incontinence with Alzheimer's Disease: Implications for Treatment.International journal of molecular sciences · 2026Article
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- Article
- Review
- Exploring Integrins in Smooth Muscle Function: Addressing Challenging Levels of Complexity and Deciphering Organ-specific Codes of Contraction?Function (Oxford, England) · 2022Article
- Functional roles for PIEZO1 and PIEZO2 in urothelial mechanotransduction and lower urinary tract interoception.JCI insight · 2021Article
- Molecular mechanisms of voiding dysfunction in a novel mouse model of acute urinary retention.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Urothelium-Specific Deletion of Connexin43 in the Mouse Urinary Bladder Alters Distension-Induced ATP Release and Voiding Behavior.International journal of molecular sciences · 2021Article
- The Urothelium: Life in a Liquid Environment.Physiological reviews · 2020Review
- Dystrophin is expressed in smooth muscle and afferent nerve fibers in the rat urinary bladder.Muscle & nerve · 2019Article
- microRNA Crosstalk Influences Epithelial-to-Mesenchymal, Endothelial-to-Mesenchymal, and Macrophage-to-Mesenchymal Transitions in the Kidney.Frontiers in pharmacology · 2019Review
- Void spot assay: recommendations on the use of a simple micturition assay for mice.American journal of physiology. Renal physiology · 2018Review
- Evaluating the voiding spot assay in mice: a simple method with complex environmental interactions.American journal of physiology. Renal physiology · 2017Article
- Stretch-induced actomyosin contraction in epithelial tubes: Mechanotransduction pathways for tubular homeostasis.Seminars in cell & developmental biology · 2017Review
- Stage- and subunit-specific functions of polycomb repressive complex 2 in bladder urothelial formation and regeneration.Development (Cambridge, England) · 2017Article
- Invasion of Host Cells and Tissues by Uropathogenic Bacteria.Microbiology spectrum · 2016Review
- Pharmacological methods for the preclinical assessment of therapeutics for OAB: an up-to-date review.International urogynecology journal · 2016Review
- Intact urothelial barrier function in a mouse model of ketamine-induced voiding dysfunction.American journal of physiology. Renal physiology · 2016Article
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8 authors at 2 institutions in 1 country.
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Abstract
Bladder urothelium senses and communicates information about bladder fullness. However, the mechanoreceptors that respond to tissue stretch are poorly defined. Integrins are mechanotransducers in other tissues. Therefore, we eliminated β1-integrin selectively in urothelium of mice using Cre-LoxP targeted gene deletion. β1-Integrin localized to basal/intermediate urothelial cells by confocal microscopy. β1-Integrin conditional-knockout (β1-cKO) mice lacking urothelial β1-integrin exhibited down-regulation and mislocalization of α3- and α5-integrins by immunohistochemistry but, surprisingly, had normal morphology, permeability, and transepithelial resistance when compared with Cre-negative littermate controls. β1-cKO mice were incontinent, as judged by random urine leakage on filter paper (4-fold higher spotting, P<0.01; 2.5-fold higher urine area percentage, P<0.05). Urodynamic function assessed by cystometry revealed bladder overfilling with 80% longer intercontractile intervals (P<0.05) and detrusor hyperactivity (3-fold more prevoid contractions, P<0.05), but smooth muscle contractility remained intact. ATP secretion into the lumen was elevated (49 vs. 22 nM, P<0.05), indicating abnormal filling-induced purinergic signaling, and short-circuit currents (measured in Ussing chambers) revealed 2-fold higher stretch-activated ion channel conductances in response to hydrostatic pressure of 1 cmH2O (P<0.05). We conclude that loss of integrin signaling from urothelium results in incontinence and overactive bladder due to abnormal mechanotransduction; more broadly, our findings indicate that urothelium itself directly modulates voiding.
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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.