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Proteomic analysis of rat penile tissue in a model of erectile dysfunction after radical prostatectomy
Author(s) -
Liu Xiaopeng,
Gao Xin,
Pang Jun,
Zhang Yan,
Wang Kebing,
Fang Youqiang,
Wen Xinqiao,
Cai Yubin
Publication year - 2007
Publication title -
bju international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.773
H-Index - 148
eISSN - 1464-410X
pISSN - 1464-4096
DOI - 10.1111/j.1464-410x.2007.06842_99_6.x
Subject(s) - pathophysiology , erectile dysfunction , proteomics , annexin , penis , neurectomy , denervation , endocrinology , medicine , prostatectomy , oxidative stress , chemistry , urology , pathology , apoptosis , surgery , prostate , biochemistry , cancer , alternative medicine , gene
OBJECTIVE To identify differential protein expression in penile tissue in a rat model of erectile dysfunction (ED) at an early stage after bilateral cavernosal nerve (CN) neurectomy, using proteomic techniques. MATERIALS AND METHODS Twelve male adult Sprague‐Dawley rats were randomly divided into two equal groups, one having bilateral CN resection and one a control group. The penises were harvested 7 days after CN resection. Total protein was separated into >1250 protein spots by two‐dimensional electrophoresis using pH 3–10 nonlinear immobilized pH gradient strips. Differential expression of proteins was analysed using matrix‐assisted laser desorption/ionization time‐of‐flight mass spectrometry and database searching. RESULTS Thirty‐two proteins were significantly changed in the denervated penis, of which 25 (including nine up‐regulated and 16 down‐regulated) with cytoskeletal functions, and pathophysiological functions related to energy metabolism and oxidative stress, were identified. Examples include transgelin, creatine kinase B, annexin‐1 and galactin‐7. CONCLUSIONS The expression of several important proteins participating in pathophysiological processes of penile tissue are changed early after bilateral CN neurectomy. These changes might give new insights into the cellular and molecular mechanisms involved in neurogenic ED development, and indicate potential therapeutic targets.