Journal of the American Society of Hypertension
Volume 1, Issue 3 , Pages 164-168, May 2007

Molecular mechanism of juxtaglomerular cell hyperplasia: a unifying hypothesis

  • Kenichi Matsushita, MD, PhD

      Affiliations

    • Mandel Center for Hypertension Research, Duke University Medical Center, Durham, North Carolina, USA
    • Cardiology Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    • ,
  • Zhiping Zhang, MD, PhD

      Affiliations

    • Mandel Center for Hypertension Research, Duke University Medical Center, Durham, North Carolina, USA
    • Cardiology Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    • ,
  • Richard E. Pratt, PhD

      Affiliations

    • Mandel Center for Hypertension Research, Duke University Medical Center, Durham, North Carolina, USA
    • Cardiology Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    • ,
  • Victor J. Dzau, MD

      Affiliations

    • Mandel Center for Hypertension Research, Duke University Medical Center, Durham, North Carolina, USA
    • Cardiology Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA
    • Corresponding Author InformationCorresponding author: Victor J. Dzau, MD, Office of the Chancellor, Duke University Medical Center, Durham, North Carolina 27710. Tel: 919-684-2255; fax: 919-681-7020.

Received 5 January 2007; accepted 19 February 2007.

Abstract 

Renin is the first enzymatic step of the renin angiotensin cascade and plays an important role in cardiovascular homeostasis. Renin is mainly expressed in and released from specialized juxtaglomerular (JG) cells in kidney. JG cells develop hyperplasia in response to various chronic stimuli while maintaining the ability to express high levels of renin. However, the molecular and cellular mechanisms of JG cell hyperplasia are unknown. Based on the authors’ previous observation that a nuclear hormone receptor, liver X receptor α, regulates renin expression as well as growth and differentiation genes such as c-myc, the authors propose the hypothesis that liver X receptor α can contribute to JG cell hyperplasia under conditions of chronic and intense induction of these genes. This hypothesis may provide a potential explanation for the observation that the JG cells can maintain a highly specialized renin-producing phenotype while undergoing hyperplasia.

Keywords: Renin, juxtaglomerular apparatus, gene expression, gene regulation

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 This study was supported by the National Heart, Lung, and Blood Institute (Grant nos. R01 HL35610, HL58516, HL72010, and HL73219 [VJD]) and the Edna Mandel Foundation (VJD).Conflict of interest: none.

PII: S1933-1711(07)00059-9

doi:10.1016/j.jash.2007.02.004

Journal of the American Society of Hypertension
Volume 1, Issue 3 , Pages 164-168, May 2007

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