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      SCI SCIE SCOPUS

      Expression of human β‐defensin‐2 in the prostate

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      https://www.riss.kr/link?id=A107563265

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      <P>We found the expression of human beta-defensin-2 (HBD-2) in the prostate for the first time and LPS, a gram negative bacterial component, upregulated HBD-2 in prostate epithelial cells. We are looking for other antimicrobial peptides expressed in the prostate besides human beta-defensin-2. Also, we are studying the relationship between antimicrobial peptides and the development or progression of prostate diseases. OBJECTIVE To investigate the expression and regulation of human beta-defensin-2 (HBD-2) in the prostate. PATIENTS AND METHODS Normal human prostate epithelial cell line (RWPE-1), human prostate cancer cell lines (DU-145, PC-3), and paraffin-embedded prostate tissue from patients with benign prostatic hyperplasia (BPH) were analysed by RT-PCR and immunohistochemical staining. HBD-2 expression was also analysed by RT-PCR and ELISA in RWPE-1 cells treated with lipopolysaccharide (LPS). Nuclear factor-kappa B (NF-kappa B) activation was assessed by I kappa B alpha immunoblotting and electrophoretic mobility shift assay (EMSA). RESULTS BPH tissue and all of the tested prostate cell lines other than PC-3 constitutively express HBD-2 mRNA. HBD-2 protein was strongly detected in prostate gland tissue surrounded by inflammatory cells including macrophages. Exposure to LPS induced HBD-2 upregulation and NF-kappa B activation, as assessed by I kappa B alpha phosphorylation and degradation in RWPE-1 cells. Bay11-7082, an NF-kappa B inhibitor prevented LPS-induced HBD-2 production in RWPE-1 cells. CONCLUSIONS Prostate epithelial cells may constitutively express HBD-2, and its expression was upregulated by LPS. Our data indicate that HBD-2 may be an important immunomodulatory factor in prostate function. Expression of HBD-2 in normal prostates and the potential role of HBD-2 in prostatitis and BPH should be addressed in the future.</P>
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      <P>We found the expression of human beta-defensin-2 (HBD-2) in the prostate for the first time and LPS, a gram negative bacterial component, upregulated HBD-2 in prostate epithelial cells. We are looking for other antimicrobial peptides expresse...

      <P>We found the expression of human beta-defensin-2 (HBD-2) in the prostate for the first time and LPS, a gram negative bacterial component, upregulated HBD-2 in prostate epithelial cells. We are looking for other antimicrobial peptides expressed in the prostate besides human beta-defensin-2. Also, we are studying the relationship between antimicrobial peptides and the development or progression of prostate diseases. OBJECTIVE To investigate the expression and regulation of human beta-defensin-2 (HBD-2) in the prostate. PATIENTS AND METHODS Normal human prostate epithelial cell line (RWPE-1), human prostate cancer cell lines (DU-145, PC-3), and paraffin-embedded prostate tissue from patients with benign prostatic hyperplasia (BPH) were analysed by RT-PCR and immunohistochemical staining. HBD-2 expression was also analysed by RT-PCR and ELISA in RWPE-1 cells treated with lipopolysaccharide (LPS). Nuclear factor-kappa B (NF-kappa B) activation was assessed by I kappa B alpha immunoblotting and electrophoretic mobility shift assay (EMSA). RESULTS BPH tissue and all of the tested prostate cell lines other than PC-3 constitutively express HBD-2 mRNA. HBD-2 protein was strongly detected in prostate gland tissue surrounded by inflammatory cells including macrophages. Exposure to LPS induced HBD-2 upregulation and NF-kappa B activation, as assessed by I kappa B alpha phosphorylation and degradation in RWPE-1 cells. Bay11-7082, an NF-kappa B inhibitor prevented LPS-induced HBD-2 production in RWPE-1 cells. CONCLUSIONS Prostate epithelial cells may constitutively express HBD-2, and its expression was upregulated by LPS. Our data indicate that HBD-2 may be an important immunomodulatory factor in prostate function. Expression of HBD-2 in normal prostates and the potential role of HBD-2 in prostatitis and BPH should be addressed in the future.</P>

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