{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,16]],"date-time":"2026-06-16T17:53:22Z","timestamp":1781632402810,"version":"3.54.5"},"reference-count":57,"publisher":"American Physiological Society","issue":"5","license":[{"start":{"date-parts":[[2022,8,24]],"date-time":"2022-08-24T00:00:00Z","timestamp":1661299200000},"content-version":"vor","delay-in-days":235,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2022,9,13]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The bladder undergoes large shape changes as it fills and empties and experiences complex mechanical forces. These forces become abnormal in diseases of the lower urinary tract such as overactive bladder, neurogenic bladder, and urinary retention. As the primary mechanosensors linking the actin cytoskeleton to the extracellular matrix (ECM), integrins are likely to play vital roles in maintaining bladder smooth muscle (BSM) homeostasis. In a tamoxifen-inducible smooth muscle conditional knockout of \u03b21-integrin, there was concomitant loss of \u03b11- and \u03b13-integrins from BSM and upregulation of \u03b1V- and \u03b23-integrins. Masson's staining showed a reduction in smooth muscle with an increase in collagenous ECM. Functionally, mice exhibited a changing pattern of urination by voiding spot assay up to 8\u2009wk after tamoxifen. By 8\u2009wk, there was increased frequency with reductions in voided volume, consistent with overactivity. Cystometrograms confirmed that there was a significant reduction in intercontractile interval with reduced maximal bladder pressure. Muscle strip myography revealed a loss of contraction force in response to electrical field stimulation, that was entirely due to the loss of muscarinic contractility. Quantitative western blotting showed a loss of M3 receptor and no change in P2X1. qPCR on ECM and interstitial genes revealed loss of Ntpd2, a marker of an interstitial cell subpopulation; and an upregulation of S100A4, which is often associated with fibroblasts. Collectively, the data show that the loss of appropriate mechanosensation through integrins results in cellular and extracellular remodeling, and concomitant bladder dysfunction that resembles lower urinary tract symptoms seen in older people.<\/jats:p>","DOI":"10.1093\/function\/zqac042","type":"journal-article","created":{"date-parts":[[2022,8,24]],"date-time":"2022-08-24T18:47:53Z","timestamp":1661366873000},"source":"Crossref","is-referenced-by-count":6,"title":["Deletion of Mechanosensory \u03b21-integrin From Bladder Smooth Muscle Results in Voiding Dysfunction and Tissue Remodeling"],"prefix":"10.1152","volume":"3","author":[{"given":"Weiqun","family":"Yu","sequence":"first","affiliation":[{"name":"Laboratory of Voiding Dysfunction, Nephrology Division, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School , Boston, MA 02215, 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