Results: Bioinformatics analysis revealed that 5 genes were significantly overexpressed in IC/BPS, and the protein-protein interaction diagram showed that BTK was a critical link between these five proteins. At the same time, functional enrichment showed that they were significantly related to innate immunity. Immunoinfiltration showed that mast cell resting in IC/BPS was significantly higher. IHC staining of clinical samples showed that the mast cell markers Tryptase and BTK were highly expressed in IC/BPS tissues. At the cell level, knockdown of BTK inhibited proliferation, migration, invasion, and degranulation of mast cells.

Conclusions: This study provides a new perspective for understanding the molecular mechanisms involved in IC/BPS and suggests that BTK may be a target for treating IC/BPS." name="description">

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Research Paper Volume 14, Issue 17 pp 7052—7064

Bruton tyrosine kinase (BTK) may be a potential therapeutic target for interstitial cystitis/bladder pain syndrome

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Figure 5. In vitro verification of the effect of BTK on the proliferation and metastasis of HMC-1 cells. (A) Western blotting displayed the knockdown efficiency of sh-BTK. (B) HMC-1 cell proliferation was detected by CCK-8 kit. (C) Wound-Healing assay showed the migration ability of HMC-1 cells. Scale bar: 100 μm. (D) Transwell assay was used to detect HCC-1 cell invasion. Scale bar: 100 μm. (E–G) Quantifications of mast cell mediators, including (E) Tryptase, (F) β-hexosaminidase and (G) Histamine. In all cases, Values are mean ± SD (n=3 for each group; *P<0.05, **P<0.01).