Ketamine Cystitis (KC) among chronic ketamine young abusers has increased dramatically and it has brought attention for Urologists. The underlying pathophysiological mechanism(s) of KC is still unclear. Therefore, the purpose of this study was to elucidate the possible pathophysiological mechanism(s) of KC through proteomic techniques.
Bladder tissues were obtained from 7 patients with KC, 7 patients with interstitial cystitis/bladder pain syndrome, and 5 control subjects who underwent videourodynamic study followed by augmentation enterocystoplasty to increase bladder capacity. 2DE/MS/MS based approach, functional classifications, and network analyses were used for proteomic and bioinformatics analyses and protein validation was carried out by Western blot analysis.
Among the proteins identified, bioinformatics analyses revealed that several actin binding related proteins such as cofilin-1, myosin light polypeptide 9, filamin A, gelsolin, lamin A were involved in the apoptosis. Besides, the contractile proteins and cytoskeleton proteins such as myosin light polypeptide 9, filamin A, and calponin were found downregulated in KC bladders.
Increased apoptosis in KC might be mediated by actin binding proteins and a Ca(2+) -activated protease. Rapid detrusor contraction in KC might be induced by contractile proteins and cytoskeleton proteins. This article is protected by copyright. All rights reserved.
Proteomics. Clinical applications. 2016 Jan 10 [Epub ahead of print]
Hsueh-Hui Yang, Wei-Jun Zhai, Hann-Chorng Kuo
Department of Medical Research, Buddhist Tzu Chi General Hospital, Hualien, 970, Taiwan., Department of Urology, Buddhist Tzu Chi General Hospital and Tzu Chi University, Hualien, 970, Taiwan.