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Endothelial Sp1/Sp3 are essential to the effect of captopril on blood pressure in male mice

Author

Listed:
  • Hanlin Lu

    (Qilu Hospital of Shandong University)

  • Xiuxin Jiang

    (Shandong University)

  • Lifan He

    (Qilu Hospital of Shandong University)

  • Xuyang Ji

    (Qilu Hospital of Shandong University)

  • Xinyun Li

    (Qilu Hospital of Shandong University)

  • Shaozhuang Liu

    (Shandong University)

  • Yuanyuan Sun

    (Qilu Hospital of Shandong University)

  • Xiaoteng Qin

    (Qilu Hospital of Shandong University)

  • Xiwen Xiong

    (Xinxiang Medical University)

  • Sjaak Philipsen

    (Erasmus MC)

  • Bo Xi

    (Shandong University)

  • Meng Zhang

    (Qilu Hospital of Shandong University)

  • Jianmin Yang

    (Qilu Hospital of Shandong University)

  • Cheng Zhang

    (Qilu Hospital of Shandong University)

  • Yun Zhang

    (Qilu Hospital of Shandong University)

  • Wencheng Zhang

    (Qilu Hospital of Shandong University)

Abstract

Endothelial dysfunction represents a major cardiovascular risk factor for hypertension. Sp1 and Sp3 belong to the specificity protein and Krüppel-like transcription factor families. They are ubiquitously expressed and closely associated with cardiovascular development. We investigate the role of Sp1 and Sp3 in endothelial cells in vivo and evaluate whether captopril, an angiotensin-converting enzyme inhibitor (ACEI), targets Sp1/Sp3 to exert its effects. Inducible endothelial-specific Sp1/Sp3 knockout mice are generated to elucidate their role in endothelial cells. Tamoxifen-induced deletion of endothelial Sp1 and Sp3 in male mice decreases the serum nitrite/nitrate level, impairs endothelium-dependent vasodilation, and causes hypertension and cardiac remodeling. The beneficial actions of captopril are abolished by endothelial-specific deletion of Sp1/Sp3, indicating that they may be targets for ACEIs. Captopril increases Sp1/Sp3 protein levels by recruiting histone deacetylase 1, which elevates deacetylation and suppressed degradation of Sp1/Sp3. Sp1/Sp3 represents innovative therapeutic target for captopril to prevent cardiovascular diseases.

Suggested Citation

  • Hanlin Lu & Xiuxin Jiang & Lifan He & Xuyang Ji & Xinyun Li & Shaozhuang Liu & Yuanyuan Sun & Xiaoteng Qin & Xiwen Xiong & Sjaak Philipsen & Bo Xi & Meng Zhang & Jianmin Yang & Cheng Zhang & Yun Zhang, 2023. "Endothelial Sp1/Sp3 are essential to the effect of captopril on blood pressure in male mice," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-41567-1
    DOI: 10.1038/s41467-023-41567-1
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    1. Hanlin Lu & Peidong Yuan & Xiaoping Ma & Xiuxin Jiang & Shaozhuang Liu & Chang Ma & Sjaak Philipsen & Qunye Zhang & Jianmin Yang & Feng Xu & Cheng Zhang & Yun Zhang & Wencheng Zhang, 2023. "Angiotensin-converting enzyme inhibitor promotes angiogenesis through Sp1/Sp3-mediated inhibition of notch signaling in male mice," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
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