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Volume 46 Issue 3
Mar.  2019
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Abstract
References
Article Navigation >  Journal of Genetics and Genomics  > 2019  >  46(3): 109-118

CPI-17-mediated contraction of vascular smooth muscle is essential for the development of hypertension in obese mice

doi: 10.1016/j.jgg.2019.02.005
  • a 

    Model Animal Research Center and MOE Key Laboratory of Model Animal and Disease Study, Nanjing University, Nanjing, 210061, China

  • b 

    Key Laboratory of MOE for Modern Teaching Technology, Shaanxi Normal University, Xi'an, 710062, China

More Information
  • Corresponding author: E-mail address: zhangxn@nicemice.cn (Xue-Na Zhang); E-mail address: zhums@nju.edu.cn (Min-Sheng Zhu)
  • Received Date: 2018-12-03
  • Accepted Date: 2019-02-20
  • Rev Recd Date: 2019-01-21
    • Available Online: 2019-03-15
  • Publish Date: 2019-03-20
    Abstract
  • Several factors have been implicated in obesity-related hypertension, but the genesis of the hypertension is largely unknown. In this study, we found a significantly upregulated expression of CPI-17 (C-kinase-potentiated protein phosphatase 1 inhibitor of 17 kDa) and protein kinase C (PKC) isoforms in the vascular smooth muscles of high-fat diet (HFD)-fed obese mice. The obese wild-type mice showed a significant elevation of blood pressure and enhanced calcium-sensitized contraction of vascular smooth muscles. However, the obese CPI-17-deficient mice showed a normotensive blood pressure, and the calcium-sensitized contraction was consistently reduced. In addition, the mutant muscle displayed an abolished responsive force to a PKC activator and a 30%–50% reduction in both the initial peak force and sustained force in response to various G protein-coupled receptor (GPCR) agonists. Our observations showed that CPI-17-mediated calcium sensitization is mediated through a GPCR/PKC/CPI-17/MLCP/RLC signaling pathway. We therefore propose that the upregulation of CPI-17-mediated calcium-sensitized vasocontraction by obesity contributes to the development of obesity-related hypertension.
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    • References(45)
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