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Related Experiment Video

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On-Chip Endothelial Inflammatory Phenotyping
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Endothelial cell (EC)-specific Ctgf/Ccn2 expression increases EC reprogramming and atherosclerosis.

Feifei Li1, Sandeep Kumar2, Anastassia Pokutta-Paskaleva1

  • 1Department of Surgery, Emory University, Atlanta, GA, USA.

Matrix Biology : Journal of the International Society for Matrix Biology
|January 16, 2025
PubMed
Summary
This summary is machine-generated.

Stiff arteries and disturbed blood flow reprogram endothelial cells, increasing connective tissue growth factor (CTGF). This pathway, more prominent in males, drives arterial remodeling and plaque vulnerability.

Keywords:
Arterial stiffeningAtherosclerotic plaqueConnective tissue growth factor/CCN2Endothelial cellsFibulin-5Flow-mediated arterial remodelingSex-differences

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Area of Science:

  • Vascular Biology
  • Biomechanics
  • Cellular Reprogramming

Background:

  • Arterial endothelial cells (ECs) respond to biomechanical cues like wall shear stress and arterial stiffness.
  • Disturbed blood flow and increased arterial stiffness are linked to inflammation and fibrosis, promoting pathological arterial remodeling.
  • Existing pathways linking disturbed flow, stiffness, and EC reprogramming remain incompletely understood.

Purpose of the Study:

  • To investigate the molecular pathways by which ECs respond to combined stiffening and disturbed flow.
  • To identify key molecular players and biomarkers involved in EC reprogramming under these pathological conditions.
  • To test the modifiability of these pathways, particularly focusing on connective tissue growth factor (CTGF).

Main Methods:

  • Utilized a partial carotid ligation model in fibulin-5 knockout (Fbln5-/-) mice to induce disturbed flow in stiffened arteries.
  • Performed biomechanical testing to assess arterial stiffness and quantified plaque formation.
  • Generated endothelial cell-specific Ctgf knockout (Ctgfecko) mice to investigate CTGF's role.
  • Validated findings using immunohistochemistry on human patient samples (carotid endarterectomy and peripheral artery disease).

Main Results:

  • Fbln5-/- arteries under disturbed flow mimicked the stiffness of diseased human arteries, inducing endothelial-to-mesenchymal transition (EndMT) in ECs.
  • Disturbed flow in stiffened Fbln5-/- arteries led to more vulnerable atherosclerotic plaques compared to wild-type (WT) controls.
  • Connective tissue growth factor (CTGF) was upregulated in ECs under aging, stiffening, and disturbed flow conditions, serving as a key biomarker.
  • Human patient samples showed increased CTGF deposition in areas of disturbed flow.
  • Male Ctgfecko mice exhibited reduced plaque area under disturbed flow and atherogenic conditions compared to WT controls.
  • Male mice showed higher CTGF expression than female mice under disturbed flow.

Conclusions:

  • Combined arterial stiffening and disturbed flow induce significant EC reprogramming and promote pathological arterial remodeling.
  • CTGF is a critical mediator and biomarker for these biomechanically driven vascular changes.
  • Targeting CTGF may offer therapeutic potential, with sex-based differences influencing its role in arterial disease progression.
  • Further research into sex-based differences in fibrotic pathways is crucial for developing targeted therapies.