Abstract

Members of the tumor necrosis factor (TNF) superfamily have been revealed to be associated with painful bladder syndrome/interstitial cystitis (PBS/IC). TNF ligand-related molecule 1A (TL1A) and its receptor, death receptor 3 (DR3), belong to the TNF superfamily and have been implicated in chronic inflammatory diseases. Bladder biopsies from 8 female patients clinically diagnosed with PBS/IC according to the National Institute for Diabetes and Digestive and Kidney Diseases criteria and 8 female bladder carcinoma control patients were investigated to test the protein and mRNA expression levels of TL1A and DR3 using western blotting and real-time RT-PCR. The protein level ratio of TL1A to β-actin (IC, 0.65±0.03 vs. controls, 0.25±0.02, P<0.001) and of its receptor DR3 to β-actin (IC, 0.66±0.06 vs. controls, 0.27±0.02, P<0.001) were observed to be significantly higher in the patients with IC. The real-time RT-PCR ΔCts of TL1A minus GAPDH (IC, 7.60±0.52 vs. controls, 10.08±0.32, P<0.001) and the DR3 minus GAPDH (IC, 6.68±0.60 vs. controls, 8.99±0.61, P=0.017) were observed to be significantly lower in the patients with IC, suggesting that the mRNA levels of TL1A and DR3 were higher in the PBS/IC patients. The protein and mRNA expression of TL1A and DR3 are upregulated in the bladder tissues of PBS/IC patients and may be involved in inflammation and apoptosis in PBS/IC.

Highlights

  • Painful bladder syndrome/interstitial cystitis (PBS/IC) is a clinical condition that mainly occurs in females

  • tumor necrosis factor (TNF) ligand‐related molecule 1A [TL1A; known as vascular endothelial growth inhibitor (VEGI) and TNFSF member 15 (TNFSF15)] is an anti‐angiogenic cytokine belonging to the TNFSF

  • The present study investigated the expression levels of TL1A and its receptor, death receptor 3 (DR3), in bladder biopsy tissues and revealed a potential link between TL1A, DR3 and PBS/IC

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Summary

Introduction

Painful bladder syndrome/interstitial cystitis (PBS/IC) is a clinical condition that mainly occurs in females. A number of studies have demonstrated a link between PBS/IC and inflammation [3,4,5,6,7]. Members of the tumor necrosis factor (TNF) superfamily (TNFSF) have been revealed to be associated with PBS/IC [6,8,9]. TL1A regulates tumor cell behavior and is involved in chronic inflammatory disease [10,11,12]. These studies collectively indicate that TL1A has a role in PBS/IC

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