Article

Spinal cord injury markedly altered protein expression patterns in the affected rat urinary bladder during healing stages.

MRCND and Department of Biochemistry, BK21 Program for Biomedical Sciences, School of Medicine and Institute of Health Sciences, Gyeongsang National University, Jinju, Korea.
Journal of Korean medical science (Impact Factor: 0.84). 06/2011; 26(6):814-23. DOI: 10.3346/jkms.2011.26.6.814
Source: PubMed

ABSTRACT The influence of spinal cord injury (SCI) on protein expression in the rat urinary bladder was assessed by proteomic analysis at different time intervals post-injury. After contusion SCI between T9 and T10, bladder tissues were processed by 2-DE and MALDI-TOF/MS at 6 hr to 28 days after SCI to identify proteins involved in the healing process of SCI-induced neurogenic bladder. Approximately 1,000 spots from the bladder of SCI and sham groups were visualized and identified. At one day after SCI, the expression levels of three protein were increased, and seven spots were down-regulated, including heat shock protein 27 (Hsp27) and heat shock protein 20 (Hsp20). Fifteen spots such as S100-A11 were differentially expressed seven days post-injury, and seven proteins including transgelin had altered expression patterns 28 days after injury. Of the proteins with altered expression levels, transgelin, S100-A11, Hsp27 and Hsp20 were continuously and variably expressed throughout the entire post-SCI recovery of the bladder. The identified proteins at each time point belong to eight functional categories. The altered expression patterns identified by 2-DE of transgelin and S100-A11 were verified by Western blot. Transgelin and protein S100-A11 may be candidates for protein biomarkers in the bladder healing process after SCI.

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    ABSTRACT: Background and purpose: The kinin B(1) and B(2) receptors have been implicated in physiological and pathological conditions of the urinary bladder. However, their role in overactive urinary bladder (OAB) syndrome following spinal cord injury (SCI) remains elusive. Experimental approach: We investigated the role played by kinin B(1) and B(2) receptors in OAB after SCI in rats. Key results: SCI was associated with a marked inflammatory response and functional changes in the urinary bladder. The SCI resulted in the B(1) R mRNA up-regulation in the urinary bladder, dorsal root ganglion and spinal cord, as well as in B(1) protein in the urinary bladder and B(1) R and B(2) R protein in the spinal cord. Interestingly, both B(1) and B(2) protein expression were similarly distributed in detrusor muscle and urothelium of SCI animals. In vitro stimulation of urinary bladder with the selective B(1) or B(2) agonist elicited a higher concentration-response curve in the SCI urinary bladder versus naive or sham urinary bladder. Cystometry studies revealed that the treatment of SCI animals with the B(2) selective antagonist Icatibant reduced the amplitude and number of non-voiding contractions (NVCs). The B(1) antagonist des-Arg(9) -[Leu(8) ]-bradykinin reduced the number of NVCs while the non-peptide B(1) antagonist SSR240612 reduced the number of NVCs, the urinary bladder capacity and increased the voiding efficiency and voided volume. Conclusions and implications: Taken together, these data showed the important roles of B(1) and B(2 ) receptors in OAB following SCI in rats and suggest that the blockade of these receptors could be potential therapeutic target for controlling OAB. © 2012 The Authors. British Journal of Pharmacology © 2012 The British Pharmacological Society.
    British Journal of Pharmacology 08/2012; · 5.07 Impact Factor

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