Down-Regulation of the Large-Conductance Ca²⁺-Activated K⁺ Channel, KCa1.1 in the Prostatic Stromal Cells of Benign Prostate Hyperplasia

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  • Niwa Satomi
    Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Ohya Susumu
    Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Kojima Yoshiyuki
    Department of Nephro-urology, Graduate School of Medical Sciences, Nagoya City University
  • Sasaki Shoichi
    Department of Nephro-urology, Graduate School of Medical Sciences, Nagoya City University
  • Yamamura Hisao
    Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University
  • Sakuragi Motomu
    Hanno Research Center, Taiho Pharmaceutical Co., Ltd.
  • Kohri Kenjiro
    Department of Nephro-urology, Graduate School of Medical Sciences, Nagoya City University
  • Imaizumi Yuji
    Department of Molecular & Cellular Pharmacology, Graduate School of Pharmaceutical Sciences, Nagoya City University

書誌事項

タイトル別名
  • Down-Regulation of the Large-Conductance Ca<sup>2+</sup>-Activated K<sup>+</sup> Channel, K<sub>Ca</sub>1.1 in the Prostatic Stromal Cells of Benign Prostate Hyperplasia

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抄録

Large-conductance Ca2+-activated K+ (BKCa) channel encoded by KCa1.1 plays an important role in the control of smooth muscle tone by modulating membrane potential and intracellular Ca2+ mobilization. BKCa channel is functionally expressed in prostatic smooth muscle cells, and is activated by α1-adrenoceptor agonists. The main objective of this study was to elucidate the pathophysiological significance of changes in prostatic KCa1.1 expressions in benign prostatic hyperplasia (BPH). Our previous study has shown that KCa3.1 encoding intermediate-conductance KCa (IKCa) channel is up-regulated in stromal cells of implanted urogenital sinuses (UGSs) of stromal hyperplasia BPH model rats and in those of prostatic tissues from BPH patients. In the present study, the results from real-time polymerase chain reaction (PCR), Western blot, and immunohistochemical analyses showed significant down-regulation of KCa1.1 transcripts and proteins and negative correlation between KCa1.1 and KCa3.1 transcript expressions in prostatic stromal cells of both BPH model rats and BPH patients. Corresponding to down-regulation of KCa1.1 expression in stromal cells of implanted UGSs, membrane depolarization by application of the BKCa channel blocker was disappeared. Down-regulation of KCa1.1 may be involved in the phenotype switch from contractile profile to proliferative one in prostatic stromal cells of BPH patients.

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