Abstract
You have accessJournal of UrologyBenign Prostatic Hyperplasia: Evaluation & Markers1 Apr 2014PD25-12 UPREGULATED CHEMOKINE EXPRESSION ASSOCIATED WITH BPH IS REPLICATED IN RAT MODEL OF NONBACTERIAL PROSTATITIS Mahendra Kashyap, Zhou Wang, Naoki Kawamorita, Yasuhito Funahashi, Kenichi Mori, Naoki Yoshimura, and Pradeep Tyagi Mahendra KashyapMahendra Kashyap More articles by this author , Zhou WangZhou Wang More articles by this author , Naoki KawamoritaNaoki Kawamorita More articles by this author , Yasuhito FunahashiYasuhito Funahashi More articles by this author , Kenichi MoriKenichi Mori More articles by this author , Naoki YoshimuraNaoki Yoshimura More articles by this author , and Pradeep TyagiPradeep Tyagi More articles by this author View All Author Informationhttps://doi.org/10.1016/j.juro.2014.02.1991AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookTwitterLinked InEmail INTRODUCTION AND OBJECTIVES Benign prostatic hyperplasia (BPH) is linked to overexpression of stromal and epithelial growth factors associated with chronic inflammation. Analysis of prostate tissue from BPH patients have identified upregulated gene expression of several chemokines including CCL2/monocyte chemoattractant protein-1 (MCP-1), CCL3/macrophage inflammatory protein-1α (MIP-1α) and CXCL1/CINC-1 (Roberts et al; Prostate 2009). The objective of this study was to evaluate whether chemokine expression noted in the tissue of human BPH patients is recapitulated in tissue and urine specimens harvested from a rat model of nonbacterial prostatitis (NBP). METHODS NBP was induced in three-month-old male Sprague-dawley rats by intraprostatic injection of 5% formalin in saline into the ventral lobes of prostate with 50μL in each lobe. Sham group was injected with same volume of saline into prostate and 7 days later, whole prostates and bladder including urine specimens collected just before sacrifice were analyzed by MILLIPLEX rat Cytokine/Chemokine assay. RESULTS NBP caused a significant decrease in prostate weight and increased the prostatic levels of the interleukins and chemokines (MCP-1, MIP-1a, CXCL-1 and CXCL-10) relative to sham group (fig.). Incidentally, chemokine expression was also significantly elevated in rat bladder given intraprosatic formalin relative to bladder of sham group. All the chemokines overexpressed in prostate and bladder were also measurable in urine collected from both groups with no significant difference. Only MIP-1a was significantly elevated in urine from NBP rat compared to urine from sham group. The tissue source of chemokines in urine could be both prostate and bladder. CONCLUSIONS The chemokine signature in prostate tissue of NBP rats corroborates the upregulated gene expression noted in prostate tissue of BPH patients. The magnitude of chemokine expression in tissue did not lead to urinary elevation for CXCl-1, CXCL-10 and MCP-1, perhaps due to their increased tissue binding with respective cognate receptors. The rat model of NBP can provide further insight into the role of inflammation in BPH progression. Although MCP-1 and MIP-1a have been measured in prostatic fluid of BPH patients, their presence in voided urine of BPH patients could be serve as a BPH biomarker. © 2014FiguresReferencesRelatedDetails Volume 191Issue 4SApril 2014Page: e730 Advertisement Copyright & Permissions© 2014MetricsAuthor Information Mahendra Kashyap More articles by this author Zhou Wang More articles by this author Naoki Kawamorita More articles by this author Yasuhito Funahashi More articles by this author Kenichi Mori More articles by this author Naoki Yoshimura More articles by this author Pradeep Tyagi More articles by this author Expand All Advertisement Advertisement PDF downloadLoading ...
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