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Molecular and Cellular Biochemistry

, Volume 455, Issue 1–2, pp 99–108 | Cite as

Overexpression of CTRP9 attenuates the development of atherosclerosis in apolipoprotein E-deficient mice

  • Chengmin Huang
  • Peng Zhang
  • Tingting Li
  • Jun Li
  • Tianjiao Liu
  • Anju Zuo
  • Jiying Chen
  • Yuan GuoEmail author
Article
  • 207 Downloads

Abstract

This study was aimed to explore the role of C1q/TNF-related protein 9 (CTRP9) on atherosclerotic lesion formation. A recombinant lentiviral vector carrying mouse CTRP9 (Lv-CTRP9) was injected intravenously into apolipoprotein E knockout (ApoE−/−) mice given a high-fat diet (HFD). CTRP9 overexpression substantially attenuated atherosclerotic lesion size of mice. The accumulation of macrophages and smooth muscle cells (SMCs) was significantly decreased in atherosclerotic regions with CTRP9 overexpression by immunohistochemical analysis. In addition, CTRP9 downregulated the expressions of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis factor-alpha (TNF-α), two main proinflammatory cytokines in atherosclerosis. Furthermore, the autophagy level remarkably increased which was presented by microtubule-associated protein light chain 3B (LC3B) conversion and sequestosome 1 (SQSTM1/p62) degradation. Further study showed that CTRP9 increased adenosine monophosphate-activated protein kinase (AMPK) phosphorylation and decreased mammalian target of rapamycin (mTOR) phosphorylation in vivo. These observations reveal that CTRP9 exerts a protecting role in early atherosclerotic lesions and its anti-atherosclerotic effect is associated with autophagy induction through AMPK/mTOR signaling pathway.

Keywords

CTRP9 Atherosclerosis Autophagy AMPK mTOR 

Notes

Acknowledgements

This work was supported by the National Natural Science Foundation of China (Grant No. 81671950) and Department of Science and Technology of Shandong Province (2014GSF118020).

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2018

Authors and Affiliations

  • Chengmin Huang
    • 1
    • 2
    • 4
  • Peng Zhang
    • 1
    • 2
    • 5
  • Tingting Li
    • 1
    • 2
    • 3
  • Jun Li
    • 1
    • 2
  • Tianjiao Liu
    • 2
  • Anju Zuo
    • 2
    • 3
  • Jiying Chen
    • 1
    • 2
    • 3
  • Yuan Guo
    • 1
    • 2
    • 3
    Email author
  1. 1.Department of CardiologyQilu Hospital of Shandong UniversityJinanPeople’s Republic of China
  2. 2.The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of HealthQilu Hospital of Shandong UniversityJinanPeople’s Republic of China
  3. 3.Department of General MedicineQilu Hospital of Shandong UniversityJinanPeople’s Republic of China
  4. 4.Department of CardiologyThe Affiliated Cardiovascular Hospital of Xiamen UniversityXiamenPeople’s Republic of China
  5. 5.Department of GeriatricsPeking University First HospitalBeijingPeople’s Republic of China

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