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Transverse Aortic Constriction in Mice
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CD9 exacerbates pathological cardiac hypertrophy through regulating GP130/STAT3 signaling pathway

Yue Li1,2, Siyuan Fan3, Lingyao Kong1

  • 1Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan 450052, China.

Iscience
|October 20, 2023
PubMed

Insights

CD9 protein exacerbates pathological cardiac hypertrophy by interacting with GP130 and activating the STAT3 pathway. Reducing CD9 expression improves cardiac function and reduces hypertrophy markers.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Biochemistry

Background:

  • CD9, a tetraspanin protein, is implicated in inflammation and cancer.
  • Its role in pathological cardiac hypertrophy remains largely unexplored.

Purpose of the Study:

  • To investigate the role of CD9 in pathological cardiac hypertrophy.
  • To elucidate the underlying molecular mechanisms involving CD9 in cardiac hypertrophy.

Main Methods:

  • Utilized a transaortic constriction (TAC) mouse model to induce cardiac hypertrophy.
  • Employed CD9 knockdown and co-immunoprecipitation assays.
  • Assessed cardiac function, heart weight, cardiomyocyte size, fibrosis, GP130 levels, and STAT3 phosphorylation.

Main Results:

  • CD9 expression was upregulated in TAC-induced myocardial tissue.
  • CD9 knockdown ameliorated cardiac dysfunction, reduced heart weight, cardiomyocyte size, and fibrosis.
  • CD9 directly binds to GP130, reducing GP130 protein levels and STAT3 phosphorylation.
  • GP130 knockdown counteracted the detrimental effects of CD9 on cardiac hypertrophy.

Conclusions:

  • CD9 exacerbates pathological cardiac hypertrophy by modulating the GP130/STAT3 signaling pathway.
  • CD9 represents a potential therapeutic target for treating pathological cardiac hypertrophy.

Keywords:
Cardiovascular medicineMolecular physiologyPathophysiology

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