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Activating transcription factor 6 protects against endothelial barrier dysfunction.

Khadeja-Tul Kubra1, Mohammad S Akhter1, Yogesh Saini2

  • 1School of Basic Pharmaceutical and Toxicological Sciences, College of Pharmacy, University of Louisiana Monroe, Monroe, LA 71201, USA.

Cellular Signalling
|August 6, 2022
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Activating ATF6, a UPR sensor, protects against lipopolysaccharides-induced endothelial barrier dysfunction, offering a potential therapeutic target for sepsis and acute respiratory distress syndrome (ARDS).

Keywords:
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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Physiology

Background:

  • Endothelial hyperpermeability is a hallmark of sepsis and acute respiratory distress syndrome (ARDS).
  • Understanding molecular pathways of barrier dysfunction is crucial for developing ARDS therapeutics.
  • The unfolded protein response (UPR) pathway, involving the ATF6 sensor, mitigates endoplasmic reticulum stress.

Purpose of the Study:

  • To investigate the role of ATF6 in lipopolysaccharides (LPS)-induced endothelial hyperpermeability.
  • To evaluate the therapeutic potential of modulating ATF6 activity in endothelial barrier dysfunction.

Main Methods:

  • In vitro study using bovine pulmonary artery endothelial cells (BPAEC) exposed to LPS.
  • Modulation of ATF6 activity using AA147 (activator) and Ceapin-A7 or siRNA (suppressor).
  • Assessment of endothelial barrier function via electric cell-substrate impedance sensing (ECIS) for transendothelial resistance (TEER) and FITC-dextran assay for paracellular permeability.

Main Results:

  • AA147, an ATF6 inducer, prevented LPS-induced barrier disruption by inhibiting Cofilin/MLC2 activation and VE-Cadherin phosphorylation.
  • AA147 treatment maintained TEER and reduced paracellular hyperpermeability in LPS-exposed cells.
  • ATF6 suppression by Ceapin-A7 or siRNA potentiated LPS-induced endothelial barrier dysfunction.

Conclusions:

  • ATF6 activation confers protection against endothelial barrier dysfunction.
  • The UPR sensor ATF6 represents a promising therapeutic target for sepsis and ARDS.