These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Increased cell apoptosis of urothelium mediated by inflammation in interstitial cystitis/painful bladder syndrome.
    Author: Shie JH, Liu HT, Kuo HC.
    Journal: Urology; 2012 Feb; 79(2):484.e7-13. PubMed ID: 22310775.
    Abstract:
    OBJECTIVE: To investigate whether bladder inflammation could directly modulate the signaling pathway of increased urothelial cell apoptosis in interstitial cystitis/painful bladder syndrome (IC/PBS). Chronic inflammation and impaired urothelial homeostasis are possible pathogenesis of IC/PBS. METHODS: A total of 29 patients with IC/PBS and 5 control patients were enrolled in the present study. Double stain, protein array analysis, and Western blotting were performed to analyze the alterations of caspase 3, Bad, Bax, phospho-p53, phospho-p38α, and tumor necrosis factor-α (TNF-α) in bladder mucosa specimens from patients with IC/PBS and control patients. The intensities of the proteins in the arrays and Western blots were quantified using ImageJ processing. Inflammatory molecule-treated urothelial cells were analyzed using terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling staining and Western blotting for the level of molecules involved in apoptosis. RESULTS: Phospho-p38 and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling double staining indicated that inflammatory and apoptotic events coexisted in the IC/PBS bladder. Protein-antibody array analysis showed that several inflammatory molecules were increased in the IC/PBS samples. We also found that the levels of pro-apoptotic proteins, including phospho-p53 (Ser 15), Bad, Bax, and cleaved caspase-3 were significantly increased in the IC/PBS bladders. These results were confirmed by immunoblotting and suggested that the tissue damage and abnormal urothelium in the IC/PBS bladder might be regulated concurrently by inflammatory signals, such as p38 mitogen-activated protein kinase and TNF-α. The in vitro analysis also showed that the apoptotic process could be induced by TNF-α treatment and anisomycin stimulation in normal urothelial cells. CONCLUSION: Apoptosis of urothelial cells in patients with IC/PBS could result from upregulation of inflammatory signals, including p38 mitogen-activated protein kinase and TNF-α.
    [Abstract] [Full Text] [Related] [New Search]