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Acid-sensing channels in human bladder: expression, function and alterations during bladder pain syndrome


Sánchez-Freire, V; Blanchard, M G; Burkhard, F C; Kessler, T M; Kellenberger, S; Monastyrskaya, K (2011). Acid-sensing channels in human bladder: expression, function and alterations during bladder pain syndrome. The Journal of Urology, 186(4):1509-1516.

Abstract

PURPOSE:

We examined the possible role of H(+) activated acid-sensing ion channels in pain perception. We characterized expression in bladder dome biopsies from patients with bladder pain syndrome and controls, in cultured human urothelium and in urothelial TEU-2 cells.
MATERIALS AND METHODS:

Cold cut biopsies from the bladder dome were obtained in 8 asymptomatic controls and 28 patients with bladder pain syndrome symptoms. Acid-sensing ion channel expression was analyzed by quantitative real-time polymerase chain reaction and immunofluorescence. Channel function was measured by electrophysiology.
RESULTS:

Acid-sensing ion channel 1a, 2a and 3 mRNA was detected in the human bladder. Similar amounts of acid-sensing ion channel 1a and 3 were detected in detrusor smooth muscle while in urothelium acid-sensing ion channel 3 levels were higher than levels of acid-sensing ion channel 1a. Acid-sensing ion channel 2a mRNA levels were lower than acid-sensing ion channel 1a and 3 levels in each layer. Acid-sensing ion channel currents were measured in TEU-2 cells and in primary cultures of human urothelium. Activated acid-sensing ion channel expression was confirmed by quantitative real-time polymerase chain reaction. TEU-2 cell differentiation caused acid-sensing ion channel 2a and 3 mRNA up-regulation, and acid-sensing ion channel 1a mRNA down-regulation. Patients with bladder pain syndrome showed up-regulation of acid-sensing ion channel 2a and 3 mRNA but acid-sensing ion channel 1a remained unchanged. In contrast, transient receptor potential vanilloid 1 mRNA was down-regulated during bladder pain syndrome. All differences were statistically significant (p <0.05).
CONCLUSIONS:

Several acid-sensing ion channel subunits are expressed in human bladder and TEU-2 cells, in which levels are regulated during urothelial differentiation. Up-regulation of acid-sensing ion channel 2a and 3 in patients with bladder pain syndrome suggests involvement in increased pain and hyperalgesia. Down-regulation of transient receptor potential vanilloid 1 mRNA might indicate that a different regulatory mechanism controls its expression in the human bladder.

Copyright © 2011 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.

PURPOSE:

We examined the possible role of H(+) activated acid-sensing ion channels in pain perception. We characterized expression in bladder dome biopsies from patients with bladder pain syndrome and controls, in cultured human urothelium and in urothelial TEU-2 cells.
MATERIALS AND METHODS:

Cold cut biopsies from the bladder dome were obtained in 8 asymptomatic controls and 28 patients with bladder pain syndrome symptoms. Acid-sensing ion channel expression was analyzed by quantitative real-time polymerase chain reaction and immunofluorescence. Channel function was measured by electrophysiology.
RESULTS:

Acid-sensing ion channel 1a, 2a and 3 mRNA was detected in the human bladder. Similar amounts of acid-sensing ion channel 1a and 3 were detected in detrusor smooth muscle while in urothelium acid-sensing ion channel 3 levels were higher than levels of acid-sensing ion channel 1a. Acid-sensing ion channel 2a mRNA levels were lower than acid-sensing ion channel 1a and 3 levels in each layer. Acid-sensing ion channel currents were measured in TEU-2 cells and in primary cultures of human urothelium. Activated acid-sensing ion channel expression was confirmed by quantitative real-time polymerase chain reaction. TEU-2 cell differentiation caused acid-sensing ion channel 2a and 3 mRNA up-regulation, and acid-sensing ion channel 1a mRNA down-regulation. Patients with bladder pain syndrome showed up-regulation of acid-sensing ion channel 2a and 3 mRNA but acid-sensing ion channel 1a remained unchanged. In contrast, transient receptor potential vanilloid 1 mRNA was down-regulated during bladder pain syndrome. All differences were statistically significant (p <0.05).
CONCLUSIONS:

Several acid-sensing ion channel subunits are expressed in human bladder and TEU-2 cells, in which levels are regulated during urothelial differentiation. Up-regulation of acid-sensing ion channel 2a and 3 in patients with bladder pain syndrome suggests involvement in increased pain and hyperalgesia. Down-regulation of transient receptor potential vanilloid 1 mRNA might indicate that a different regulatory mechanism controls its expression in the human bladder.

Copyright © 2011 American Urological Association Education and Research, Inc. Published by Elsevier Inc. All rights reserved.

Citations

14 citations in Web of Science®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Balgrist University Hospital, Swiss Spinal Cord Injury Center
Dewey Decimal Classification:610 Medicine & health
Language:English
Date:2011
Deposited On:21 Feb 2012 19:36
Last Modified:05 Apr 2016 15:39
Publisher:Elsevier
ISSN:0022-5347
Publisher DOI:10.1016/j.juro.2011.05.047
PubMed ID:21855903

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