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Mechanosensitive FHL2 tunes endothelial function.

Shailaja Seetharaman1,2,3, John Devany1,2,3, Ha Ram Kim4,5

  • 1Department of Physics, The University of Chicago, Chicago, IL 60637, USA.

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|July 1, 2024
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Summary

Endothelial cells sense blood flow, but how this leads to cardiovascular disease is unclear. This study reveals Four-and-a-half LIM protein 2 (FHL2) is key in flow-induced endothelial dysfunction and atherosclerosis progression.

Keywords:
actomyosinendotheliumfluid shear stressmechanotransductionmicrotubule

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Area of Science:

  • Cardiovascular Biology
  • Mechanobiology
  • Molecular Biology

Background:

  • Endothelial cells are vital mechanosensors in blood vessels, adapting to mechanical forces.
  • Dysfunctional endothelial mechanoresponses contribute to cardiovascular diseases like atherosclerosis.
  • Mechanisms linking mechanical cues to endothelial dysfunction remain poorly understood.

Purpose of the Study:

  • To investigate how flow-mediated transcriptional regulation drives endothelial mechanoresponses.
  • To identify novel mechanosensitive genes in healthy and atherosclerotic-prone conditions.
  • To elucidate the role of Four-and-a-half LIM protein 2 (FHL2) in endothelial response to disturbed flow.

Main Methods:

  • Bulk RNA sequencing to identify mechanosensitive genes under healthy unidirectional flow (UF) and disturbed flow (DF).
  • In vitro and in vivo studies to assess FHL2 expression and function.
  • Analysis of FHL2's interaction with actin, its effect on adherens junctions, tissue permeability, and the Rho-ROCK pathway.

Main Results:

  • Novel mechanosensitive genes were identified in response to UF and DF.
  • FHL2 expression is upregulated in athero-prone DF.
  • Exogenous FHL2 expression induces discontinuous adherens junctions, increased permeability, and activates the Rho-ROCK pathway via force-dependent mechanisms.

Conclusions:

  • FHL2 is a critical mediator of endothelial mechanoresponses to disturbed flow.
  • Force-dependent FHL2 localization to stress fibers promotes hypercontractility and tissue permeability, hallmarks of atherosclerosis.
  • This study uncovers a novel mechanochemical feedback loop involving FHL2 in cardiovascular disease progression.