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Long Non-coding RNA PEBP1P2 Suppresses Proliferative VSMCs Phenotypic Switching and Proliferation in Atherosclerosis

Xingqiang He1, Zhexun Lian2, Yanyan Yang3

  • 1Department of Cardiology, The Affiliated Hospital of Qingdao University, Qingdao 266000, Shandong, P.R. China; Department of Cardiology, The Second Affiliated Hospital of Shaanxi University of Chinese Medicine, Xianyang 712000, Shaanxi, P.R. China.

Molecular Therapy. Nucleic Acids
|September 11, 2020
PubMed

Insights

A novel long non-coding RNA, PEBP1P2, was found to inhibit vascular smooth muscle cell (VSMC) proliferation and migration. PEBP1P2 may serve as a therapeutic target for cardiovascular diseases like atherosclerosis.

Area of Science:

  • Molecular Biology
  • Cardiovascular Research
  • Genetics

Background:

  • Vascular smooth muscle cell (VSMC) dysfunction is central to cardiovascular diseases (CVDs) and atherosclerosis.
  • Abnormal VSMC proliferation and phenotypic switching are key drivers of atherosclerotic plaque development.

Purpose of the Study:

  • To identify and characterize a novel long non-coding RNA (lncRNA), PEBP1P2, involved in VSMC regulation.
  • To elucidate the role of PEBP1P2 in VSMC phenotypic switching, proliferation, and migration.
  • To investigate the clinical relevance and therapeutic potential of PEBP1P2 in CVDs.

Main Methods:

  • Utilized a rat balloon injury model to assess PEBP1P2 expression in pathological arteries.
  • Investigated PEBP1P2's function in VSMC proliferation and phenotype switching induced by platelet-derived growth factor BB (PDGF-BB).
  • Confirmed cyclin-dependent kinase 9 (CDK9) as a direct target of PEBP1P2 using molecular assays.
  • Analyzed PEBP1P2 expression in serum from coronary heart disease (CHD) patients and human atherosclerotic plaques.
  • Evaluated the in vivo effect of PEBP1P2 overexpression on neointima formation and VSMC switching.

Main Results:

  • PEBP1P2 expression was significantly decreased in proliferating VSMCs and in pathological arteries.
  • PEBP1P2 suppressed VSMC proliferation, migration, and dedifferentiation.
  • PEBP1P2 directly binds to and inhibits CDK9, a key mediator of VSMC proliferation and phenotypic switching.
  • Reduced PEBP1P2 levels were observed in CHD patients' serum and atherosclerotic plaques.
  • Overexpression of PEBP1P2 attenuated neointima formation and VSMC phenotypic switching in vivo.

Conclusions:

  • PEBP1P2 acts as a critical suppressor of VSMC proliferation and migration by targeting CDK9.
  • PEBP1P2 holds significant potential as a therapeutic target for proliferative vascular diseases, including atherosclerosis.
  • PEBP1P2's dysregulation in CVD patients highlights its clinical relevance.
Keywords:
CDK9cardiovascular diseaseslong non-coding RNAsphenotypic switchingvascular smooth muscle cells

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