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Epsins Negatively Regulate Aortic Endothelial Cell Function by Augmenting Inflammatory Signaling.

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  • 1Vascular Biology Program, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.

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|August 27, 2021
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Summary
This summary is machine-generated.

Endothelial epsins 1 and 2 promote atherosclerosis by amplifying inflammatory signals. Deleting these proteins in mice reduced inflammation, suggesting epsins are key therapeutic targets for treating endothelial inflammation in atherosclerosis.

Keywords:
MCP-1TLR2/4adaptor proteinadhesion moleculeatherosclerosisendocytosisendothelial activationepsininflammationselectinvascular disease

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Area of Science:

  • Endothelial cell biology
  • Immunology
  • Cardiovascular research

Background:

  • Endothelial epsins 1 and 2 are implicated in atherosclerosis via regulating inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) degradation.
  • The precise mechanisms of epsin-mediated endothelial cell activation and inflammation require further elucidation.

Purpose of the Study:

  • To identify additional targets of epsin-mediated endothelial cell activation and inflammation.
  • To investigate the role of epsins in both acute and chronic inflammatory responses in atherosclerosis.

Main Methods:

  • Utilized ApoE-/- mice and a specialized EC-iDKO/ApoE-/- mouse model with endothelial cell-specific deletion of epsin 1 and global deletion of epsin 2.
  • Isolated murine aortic endothelial cells (MAECs) for in vitro analysis of inflammatory signaling.
  • Examined inflammatory responses to acute (TNFα, LPS) and chronic (oxLDL) stimuli.

Main Results:

  • Epsin deficiency in EC-iDKO/ApoE-/- mice and MAECs significantly abrogated inflammatory signaling under both acute and chronic stimulation.
  • Mechanistically, the epsin ubiquitin-interacting motif (UIM) was found to bind Toll-like receptors (TLR) 2 and 4, potentiating inflammatory pathways.
  • Deletion of the epsin UIM diminished this interaction, highlighting its functional importance.

Conclusions:

  • Endothelial epsin adaptor proteins significantly potentiate endothelial cell activation in models of atherogenesis.
  • These findings identify epsins as critical mediators of endothelial inflammation and potential therapeutic targets for atherosclerosis.