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Evaluation of Bioenergetic Function in Cerebral Vascular Endothelial Cells
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Succinate Regulates Endothelial Mitochondrial Function and Barrier Integrity.

Reham Atallah1, Juergen Gindlhuber2, Wolfgang Platzer1

  • 1Otto Loewi Research Center for Vascular Biology, Immunology and Inflammation, Division of Pharmacology, Medical University of Graz, 8010 Graz, Austria.

Antioxidants (Basel, Switzerland)
|January 8, 2025
PubMed
Summary
This summary is machine-generated.

Elevated succinate impairs endothelial cell mitochondrial function and barrier integrity acutely. However, cells recover over time, involving VEGF and prostaglandin pathways, with ascorbic acid offering protection.

Keywords:
barrier integrityendothelial cellsmitochondrial functionreactive oxygen speciessuccinate

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Pathophysiology

Background:

  • Endothelial dysfunction is linked to pathological conditions like cancer and cardiovascular disease.
  • Perturbed TCA cycle and succinate accumulation are observed in these conditions.
  • The role of succinate in inflammation is recognized, but its effect on endothelial cells is unclear.

Purpose of the Study:

  • To investigate how elevated intracellular succinate affects endothelial cell function and phenotype.
  • To explore the mechanisms underlying succinate-induced changes in endothelial cells.

Main Methods:

  • In vitro functional assays using primary human umbilical vein endothelial cells (HUVECs).
  • Stimulation with diethyl succinate (DES), a cell-permeable succinate analogue.
  • MTS assay, ROS measurement, mitochondrial membrane potential assessment, Seahorse mito-stress testing, Western blotting, gene expression analysis, and endothelial barrier permeability assays.

Main Results:

  • DES acutely reduced metabolic activity, increased ROS, and decreased mitochondrial membrane potential in HUVECs.
  • DES lowered oxygen consumption rate, maximal respiration, and ATP production.
  • DES induced acute endothelial barrier permeability and altered cell morphology, but cells showed recovery with sprouting and barrier restoration overnight.
  • Succinate-induced changes involved transient ERK1/2 phosphorylation changes, a mixed apoptotic/survival gene expression profile, and upregulation of VEGF.
  • Barrier restoration was mediated by COX-2/PGE2/EP4 signaling, and ascorbic acid prevented acute barrier disruption.

Conclusions:

  • Succinate significantly regulates endothelial mitochondrial function and barrier integrity.
  • Endothelial cells exhibit a counterbalancing response involving VEGF and prostaglandin production.
  • Ascorbic acid can prevent acute succinate-induced endothelial barrier disruption.