ArticleScientific reports2026
Role of Bruton's Tyrosine Kinase in mast cell driven urothelial barrier injury in an LL-37 induced model of interstitial cystitis.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic urinary disorder with unclear pathogenesis. Previous studies identified BTK as a hub gene potentially involved in IC/BPS. This study investigates BTK's role in mast cell (MC) activation and bladder inflammation. An LL-37-induced IC/BPS rat model and an in vitro MCs Co-culture system were established. BTK expression was modulated via adenoviral vectors and cell transfection. Bladder inflammation, MC degranulation, and urothelial barrier function were assessed using histology, ELISA, RT-qPCR, Western blot, IHC, TEM, and IF. MC function was evaluated via CCK-8, flow cytometry, Transwell, and TEM. LL-37 upregulated BTK in IC/BPS rats, promoting inflammation, cytokine release, collagen deposition, MC degranulation, and urothelial damage. BTK overexpression exacerbated, while knockdown alleviated these effects. In vitro, LL-37 stimulated MC proliferation, invasion, and degranulation, and reduced apoptosis. Co-culture with activated MCs decreased glycosaminoglycan (GAG) and tight junction (TJ) proteins in SV-HUC-1 cells, enhanced by BTK overexpression and reversed by knockdown. BTK promotes LL-37-induced MC activation and urothelial barrier disruption by suppressing GAGs and TJ proteins, contributing to IC/BPS pathophysiology.
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