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The decrease in histone methyltransferase EZH2 in response to fluid shear stress alters endothelial gene expression

Monika Maleszewska1,2, Byambasuren Vanchin3, Martin C Harmsen3

  • 1Cardiovascular Regenerative Medicine Research Group, Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Hanzeplein 1 (EA11), 9713 GZ, Groningen, The Netherlands. m.maleszewska@gmail.com.

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Summary

High fluid shear stress (FSS) reduces EZH2, activating protective MAPK7 signaling and promoting endothelial cell quiescence. This epigenetic regulation by EZH2 is crucial for FSS-mediated atheroprotection.

Keywords:
ChromatinEndothelial cellEnhancer of zeste homolog-2 (EZH2)Fluid shear stress (FSS)Mechanotransduction

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Area of Science:

  • Endothelial cell biology
  • Epigenetics
  • Mechanotransduction

Background:

  • High fluid shear stress (FSS) protects against atherosclerosis by preserving endothelial cell phenotype and function.
  • Mechanotransduction pathways, like MAPK7 (Erk5), are activated by FSS, but the epigenetic integration of these signals is unclear.
  • Polycomb methyltransferase EZH2's role in endothelial response to FSS is unknown.

Purpose of the Study:

  • To investigate the involvement of EZH2 in the endothelial response to FSS.
  • To elucidate the epigenetic mechanisms by which FSS exerts its atheroprotective effects.

Main Methods:

  • Human endothelial cells were subjected to FSS.
  • EZH2 expression and MAPK7 signaling were analyzed.
  • EZH2 knockdown and RNA-sequencing were performed to assess transcriptomic changes.
  • Bioinformatic analyses, including Gene Ontology, were used to identify gene networks.

Main Results:

  • FSS significantly decreased EZH2 expression in endothelial cells.
  • EZH2 knockdown activated MAPK7 signaling independently of FSS and inhibited endothelial proliferation, suggesting cell cycle arrest.
  • FSS-induced decrease in EZH2 correlated with reduced expression of cell cycle genes and a shift towards endothelial quiescence.

Conclusions:

  • EZH2 is a key FSS-responsive epigenetic regulator in endothelial cells.
  • Reduced EZH2 levels under FSS enhance atheroprotective MAPK7 signaling and promote endothelial quiescence.
  • EZH2 plays a critical role in mediating the protective effects of FSS on the endothelium.