Related Experiment Video

Updated: May 16, 2025

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation
08:43

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

Published on: May 31, 2016

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C/EBPβ activation in vascular smooth muscle cells promotes hyperlipidemia-induced phenotypic transition and arterial

Jun Ma1, Xiangyu Yang1, Yanan Li1

  • 1Department of Cardiology, West China Hospital, Sichuan University, Sichuan, China.

Signal Transduction and Targeted Therapy
|April 1, 2025
PubMed

Insights

CCAAT/enhancer-binding protein β (C/EBPβ) activation drives vascular smooth muscle cell changes, contributing to arterial stiffness in hyperlipidemia. This protein may offer new therapeutic targets and biomarkers for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Vascular Cell Biology

Background:

  • Arterial stiffness is a key risk factor for cardiovascular events, lacking specific clinical targets.
  • Hyperlipidemia is strongly linked to arterial stiffness, with elevated CCAAT/enhancer-binding protein β (C/EBPβ) observed in atherosclerotic arteries.
  • The role of C/EBPβ in vascular smooth muscle cells (VSMCs) during hyperlipidemia was previously unknown.

Purpose of the Study:

  • To investigate the role of C/EBPβ in VSMCs under hyperlipidemic conditions.
  • To elucidate the molecular mechanisms linking hyperlipidemia, VSMC changes, and arterial stiffness.
  • To identify potential therapeutic targets and biomarkers for hyperlipidemia-induced arterial stiffness.

Main Methods:

  • Examined cholesterol-induced phenotypic transition of VSMCs in vitro.
  • Analyzed C/EBPβ expression and activation in relation to cytoskeletal regulation via Disheveled-associated activator of morphogenesis 1 (Daam1).
  • Utilized conditional knockout of C/EBPβ in VSMCs of ApoE-/- mice to assess effects on vascular remodeling and pulse wave velocity.
  • Correlated C/EBPβ-regulated platelet-derived growth factor-CC (PDGF-CC) with human brachial-ankle pulse wave velocity.

Main Results:

  • Cholesterol induced a VSMC transition to macrophage-like cells, associated with C/EBPβ upregulation and activation.
  • C/EBPβ activation, linked to Daam1 and cytoskeletal regulation, promoted VSMC phenotypic switching.
  • Conditional C/EBPβ knockout in ApoE-/- mice reduced vascular remodeling and aortic pulse wave velocity.
  • Elevated PDGF-CC, regulated by C/EBPβ, correlated with human brachial-ankle pulse wave velocity.

Conclusions:

  • C/EBPβ activation promotes VSMC transition to a macrophage-like phenotype, contributing to hyperlipidemia-induced arterial stiffness.
  • PDGF-CC is a potential biomarker for arterial stiffness in humans.
  • This study reveals key molecular pathways and potential targets for managing arterial stiffness in hyperlipidemia.

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