Details

Autor(en) / Beteiligte

• Sánchez-Freire, Verónica
• Blanchard, Maxime G
• Burkhard, Fiona C
• Kessler, Thomas M
• Kellenberger, Stephan
• Monastyrskaya, Katia

Titel

Acid-Sensing Channels in Human Bladder: Expression, Function and Alterations During Bladder Pain Syndrome

Ist Teil von

• The Journal of urology, 2011-10, Vol.186 (4), p.1509-1516

Ort / Verlag

New York, NY: Elsevier Inc

Erscheinungsjahr

2011

Link zum Volltext

Quelle

MEDLINE

Beschreibungen/Notizen

• 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.