Scholarlink

<p>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.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Role of Bruton’s Tyrosine Kinase in mast cell driven urothelial barrier injury in an LL-37 induced model of interstitial cystitis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年4月30日

查看全文
  • Guang Wang,
  • Bin-sen Li,
  • Jin-yi Chu,
  • Xian Chen,
  • Tong-xin Yang,
  • Ke-wei Fang,
  • Jiong-ming Li

摘要

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.