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Updated: Mar 21, 2026

Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice
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Quantitative Analysis of Cellular Composition in Advanced Atherosclerotic Lesions of Smooth Muscle Cell Lineage-Tracing Mice

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Activation of the pluripotency factor OCT4 in smooth muscle cells is atheroprotective

Olga A Cherepanova1, Delphine Gomez1,2, Laura S Shankman1,2

  • 1Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, Virginia, USA.

Nature Medicine
|May 17, 2016
PubMed

Insights

The embryonic stem cell factor OCT4 plays a crucial role in smooth muscle cells (SMCs). Its absence in mice led to less stable atherosclerotic plaques, indicating OCT4

Area of Science:

  • Cardiovascular Biology
  • Stem Cell Biology
  • Atherosclerosis Research

Background:

  • The role of OCT4, an embryonic stem cell (ESC) pluripotency factor, in somatic cells has been controversial.
  • Previous studies have not definitively established a functional role for OCT4 in non-stem cells.

Purpose of the Study:

  • To investigate the functional role of OCT4 in smooth muscle cells (SMCs) within the context of atherosclerosis.
  • To determine the impact of OCT4 knockout in SMCs on atherosclerotic plaque development and stability.

Main Methods:

  • SMC-specific conditional knockout of Oct4 in Apoe(-/-) mice.
  • Analysis of atherosclerotic lesion size and composition.
  • SMC-lineage tracing studies.
  • Investigation of OCT4 promoter hydroxymethylation and regulatory factors (HIF-1α, KLF4).

Main Results:

  • Conditional knockout of Oct4 in SMCs led to increased atherosclerotic lesion size and decreased plaque stability.
  • Observed changes included a thinner fibrous cap, larger necrotic core, and increased intraplaque hemorrhage.
  • Reduced SMC numbers within lesions and fibrous caps, potentially due to impaired SMC migration, were noted.
  • OCT4 reactivation in SMCs correlated with promoter hydroxymethylation and was dependent on HIF-1α and KLF4.

Conclusions:

  • This study provides the first direct evidence for a functional role of OCT4 in somatic cells, specifically SMCs.
  • OCT4 is implicated in maintaining SMC number and function, influencing atherosclerotic plaque stability.
  • These findings highlight the potential significance of OCT4 in both normal and diseased somatic cells.

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