Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Investigation of early protein changes in the urinary bladder following partial bladder outlet obstruction by proteomic approach.

Authors: Kim, HJ  Sohng, I  Kim, DH  Lee, DC  Hwang, CH  Park, JY  Ryu, JW 
Citation: Kim HJ, etal., J Korean Med Sci. 2005 Dec;20(6):1000-5.
Pubmed: (View Article at PubMed) PMID:16361812
DOI: Full-text: DOI:10.3346/jkms.2005.20.6.1000

We investigated the pathophysiological mechanism by proteomic approach as a possible tool to detect the marker proteins to develop lower urinary tract symptoms following bladder outlet obstruction (BOO). Rats were randomized into 3 groups; control, sham operation and BOO groups. BOO group was divided into 1, 3, and 5 day-group. Conventional proteomics was performed with high resolution 2-D gel electrophoresis followed by computational image analysis and protein identification using mass spectrometry using rat urinary bladders. A comparison of bladder of BOO group with control bladder showed that three proteins of optineurin, thioredoxin and preprohaptoglobin were over-expressed in the bladder of BOO group. In addition, four proteins, such as peroxiredoxin 2, transgelin, hippocampal cholinergic neurostimulating peptide (HCNP) and beta-galactoside-binding lectin, were under-expressed in the bladder of BOO group. These data supported that downregulation of HCNP might make detrusor muscle be supersensitive to acetylcholine, up-regulation of optineurin means the protection of nerve injury, and down-regulation of transgelin means the decreased contractility of detrusor muscle. Beside these proteins, other proteins are related to oxidative stress or have a nonspecific function in this study. However more information is needed in human bladder tissue for clinical usage.


Disease Annotations
Objects Annotated

Additional Information

CRRD Object Information
CRRD ID: 7775024
Created: 2013-12-30
Species: All species
Last Modified: 2013-12-30
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.