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Related Experiment Video

Updated: Feb 15, 2026

Determination of Lipid Raft Partitioning of Fluorescently-tagged Probes in Living Cells by Fluorescence Correlation Spectroscopy FCS
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HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular

Prashanth Thevkar Nagesh1, Shruti Rawal2, Hitoo Nishi2

  • 1Department of Medicine, Division of Cardiology, and Cardiovascular Research Center, New York University Grossman School of Medicine, New York, New York, USA; Department of Microbiology, New York University Grossman School of Medicine, New York, New York, USA.

JACC. Basic to Translational Science
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Summary

High cholesterol causes vascular smooth muscle cells (VSMCs) to adopt harmful macrophage-like traits. Cholesterol efflux via high-density lipoprotein (HDL) can reverse this transition, suggesting HDL as a potential therapy for atherosclerosis.

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HDLlipid rafts. TGFβ signalingvascular smooth muscle cells

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Area of Science:

  • Cardiovascular Biology
  • Atherosclerosis Pathogenesis
  • Cellular Phenotypic Plasticity

Background:

  • Macrophage-like cells in atherosclerotic plaques are increasingly recognized as originating from vascular smooth muscle cells (VSMCs).
  • The phenotypic switch of VSMCs to a macrophage-like state is associated with adverse atherosclerotic progression.

Purpose of the Study:

  • To elucidate the mechanism by which cholesterol influences VSMC phenotype in atherosclerosis.
  • To investigate the potential of high-density lipoprotein (HDL)-mediated cholesterol efflux as a therapeutic strategy to restore VSMC phenotype.

Main Methods:

  • In vitro studies using human VSMCs (hVSMCs) to assess TGFβ signaling, receptor localization in lipid rafts, and gene expression (Acta2, CD68, Mir145).
  • In vivo experiments involving ApoA1 administration to atherosclerotic mice to evaluate phenotypic changes in VSMCs within plaques.

Main Results:

  • Cholesterol accumulation impairs TGFβ signaling in hVSMCs by altering TGFβ receptor localization, leading to a pro-macrophage phenotype (increased CD68, decreased Acta2).
  • HDL-mediated cholesterol efflux restored TGFβ signaling, promoting Mir145 expression and reverting VSMCs to a contractile phenotype (increased Acta2, decreased CD68).
  • In vivo ApoA1 treatment in mice mirrored these findings, enhancing VSMC Acta2 expression and reducing CD68 expression in atherosclerotic plaques.

Conclusions:

  • Cholesterol accumulation drives VSMC transition to a macrophage-like phenotype via TGFβ pathway dysregulation.
  • Cholesterol efflux mediated by HDL particles can reverse this detrimental phenotypic switch.
  • Efflux-competent HDL represents a promising therapeutic avenue for modulating VSMC phenotype in atherosclerosis.