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

Guang Wang1, , Tong-Xin Yang2, , Jiong-Ming Li2, , Zi-Ye Huang2, , Wen-Bo Yang1, , Pei Li2, , Da-Lin He1, ,

  • 1 Department of Urology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710061, Shanxi, China
  • 2 Department of Urology, The Second Affiliated Hospital of Kunming Medical University, Kunming 650101, Yunnan, China

Received: May 23, 2022       Accepted: August 24, 2022       Published: September 5, 2022
How to Cite

Copyright: © 2022 Wang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


Aims: To determine the potential diagnostic and therapeutic targets of Interstitial Cystitis/Bladder Pain Syndrome (IC/BPS).

Methods: We selected the GSE11783, GSE57560 and GSE621 datasets from the GEO database and merged them. R software was used to screen differentially expressed genes (DEGs) between IC/BPS and normal bladder tissues. The "String" online tool is used to analyze DEGs interaction and functional protein enrichment. CIBERSORT online tool was used to analyze the infiltration of immune cells. In addition, we verified the function of BTK in IC/BPS at the clinical samples and cells level.

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.


IC/BPS: Interstitial Cystitis/Bladder Pain Syndrome; DEGs: differentially expressed genes; BTK: Bruton tyrosine kinase; PPI: protein-protein interaction; NC: normal control.