The Journal of urology · 1998
Alterations in constituent urinary proteins in response to bladder outlet obstruction in rats.
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Burns J A, Kreder K J, Lubaroff D M, See W A
Аннотация
PURPOSE: Benign prostatic hyperplasia, resulting in bladder outflow obstruction, induces well recognized clinical symptoms and morphologic bladder changes. Despite these phenomenon, relatively little is known with regard to the precise molecular events occurring in the bladder as a consequence of obstruction. In an effort to screen for alterations in bladder gene expression induced by obstruction, and/or alterations in uroepithelial integrity, this study compared pre- and post-obstructive constituent urinary proteins in an animal model.
MATERIALS AND METHODS: Outlet obstruction was created using a previously established model system. Experimental animals were surgically obstructed for either 2 or 7 days, at which time the urine was aspirated and the bladders removed and weighed. Urinary proteins were separated using 2-D PAGE. Following comparison of sham versus experimental animals, microsequencing was performed on proteins that were down regulated.
RESULTS: Duplicate experiments confirmed the presence of outflow obstruction. Statistically significant increases (p <0.01) in bladder weights were seen at 2 and 7 days in the obstructed groups as compared with both sham and control groups. 2-D PAGE demonstrated a down regulation of three urinary proteins post-obstruction. Microsequencing identified these proteins as prostatic steroid-binding protein C3 precursor (pI=5.5, MW=15000), glandular kallikrein 9 (S3) precursor (pI=6.2, MW=19000), and glandular kallikrein 8 (P1) precursor (pI=6.2, MW=33000).
CONCLUSIONS: Bladder outflow obstruction alters constituent urinary protein composition in an animal model system. The precise etiology of these alterations remains to be defined.
MATERIALS AND METHODS: Outlet obstruction was created using a previously established model system. Experimental animals were surgically obstructed for either 2 or 7 days, at which time the urine was aspirated and the bladders removed and weighed. Urinary proteins were separated using 2-D PAGE. Following comparison of sham versus experimental animals, microsequencing was performed on proteins that were down regulated.
RESULTS: Duplicate experiments confirmed the presence of outflow obstruction. Statistically significant increases (p <0.01) in bladder weights were seen at 2 and 7 days in the obstructed groups as compared with both sham and control groups. 2-D PAGE demonstrated a down regulation of three urinary proteins post-obstruction. Microsequencing identified these proteins as prostatic steroid-binding protein C3 precursor (pI=5.5, MW=15000), glandular kallikrein 9 (S3) precursor (pI=6.2, MW=19000), and glandular kallikrein 8 (P1) precursor (pI=6.2, MW=33000).
CONCLUSIONS: Bladder outflow obstruction alters constituent urinary protein composition in an animal model system. The precise etiology of these alterations remains to be defined.