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Flow-dependent YAP/TAZ activities regulate endothelial phenotypes and atherosclerosis.

Kuei-Chun Wang1, Yi-Ting Yeh1, Phu Nguyen1

  • 1Institute of Engineering in Medicine and Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093.

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Disturbed blood flow activates YAP/TAZ proteins, promoting endothelial dysfunction and atherosclerosis. Inhibiting YAP/TAZ shows promise as a therapeutic strategy against atherosclerotic lesion development.

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Area of Science:

  • Cardiovascular Biology
  • Mechanobiology
  • Endothelial Cell Biology

Background:

  • Atherosclerosis is linked to hemodynamic forces.
  • Yes-associated protein (YAP) and transcriptional coactivator with PDZ-binding motif (TAZ) mediate mechanotransduction and vascular homeostasis.

Purpose of the Study:

  • Investigate YAP/TAZ roles in flow-regulated atheroprone endothelial phenotypes.
  • Determine YAP/TAZ involvement in atherosclerotic lesion development.

Main Methods:

  • Cultured endothelial cells exposed to disturbed and laminar flow.
  • En face analysis of mouse arteries.
  • YAP/TAZ knockdown and overexpression studies.
  • In vivo morpholino oligo treatment.

Main Results:

  • Disturbed flow activates YAP/TAZ, upregulating target genes (CYR61, CTGF, ANKRD1) in endothelial cells.
  • Laminar flow suppresses YAP/TAZ activity.
  • Increased nuclear YAP/TAZ and target genes observed in atheroprone arterial regions.
  • YAP/TAZ modulation affected endothelial proliferation and inflammation.
  • Statin treatment and in vivo YAP/TAZ blockade reduced atherosclerotic lesion development.

Conclusions:

  • Disturbed flow-induced YAP/TAZ activation critically promotes atheroprone phenotypes.
  • YAP/TAZ inhibition represents a potential therapeutic strategy for atherosclerosis.