Endothelial Plasticity: Shifting Phenotypes through Force Feedback

Guido Krenning, Valerio G. Barauna, Jose E. Krieger, Martin C. Harmsen, Jan-Renier A. J. Moonen*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

33 Citations (Scopus)
392 Downloads (Pure)

Abstract

The endothelial lining of the vasculature is exposed to a large variety of biochemical and hemodynamic stimuli with different gradients throughout the vascular network. Adequate adaptation requires endothelial cells to be highly plastic, which is reflected by the remarkable heterogeneity of endothelial cells in tissues and organs. Hemodynamic forces such as fluid shear stress and cyclic strain are strong modulators of the endothelial phenotype and function. Although endothelial plasticity is essential during development and adult physiology, proatherogenic stimuli can induce adverse plasticity which contributes to disease. Endothelial-to-mesenchymal transition (EndMT), the hallmark of endothelial plasticity, was long thought to be restricted to embryonic development but has emerged as a pathologic process in a plethora of diseases. In this perspective we argue how shear stress and cyclic strain can modulate EndMT and discuss how this is reflected in atherosclerosis and pulmonary arterial hypertension.

Original languageEnglish
Article number9762959
Number of pages15
JournalStem cells international
Volume2016
DOIs
Publication statusPublished - 2016

Keywords

  • FLUID SHEAR-STRESS
  • TO-MESENCHYMAL TRANSITION
  • GROWTH-FACTOR-BETA
  • PULMONARY ARTERIAL-HYPERTENSION
  • KRUPPEL-LIKE FACTOR-4
  • SMOOTH-MUSCLE-CELLS
  • ERK5 TRANSCRIPTIONAL ACTIVITY
  • GENE-EXPRESSION PROFILE
  • SAPHENOUS-VEIN GRAFTS
  • II TYPE-1 RECEPTOR

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