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Functional Differences Between Typical and Multinucleated Endothelial Cells Under Low-Density Lipoprotein Exposure.

Vadim Cherednichenko1, Diana Kiseleva1,2, Ulyana Khovantseva1,3

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This summary is machine-generated.

Multinucleated variant endothelial cells (MVECs) show increased cholesterol buildup and inflammation compared to typical endothelial cells (TECs). These findings suggest MVECs may worsen chronic endothelial dysfunction and vascular inflammation in atherosclerosis.

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Area of Science:

  • Endothelial cell biology
  • Vascular homeostasis
  • Cardiovascular disease pathogenesis

Background:

  • Endothelial cell dysfunction is central to atherosclerosis and cardiovascular diseases.
  • Multinucleated variant endothelial cells (MVECs) are found in pathological vascular regions but are poorly understood.
  • Understanding MVEC function is crucial for elucidating mechanisms of vascular disease.

Purpose of the Study:

  • To compare lipid handling, inflammatory activation, barrier function, and secretory profiles of MVECs versus typical endothelial cells (TECs).
  • To investigate the impact of low-density lipoprotein (LDL) exposure on these endothelial cell phenotypes.
  • To characterize MVECs as a distinct endothelial cell phenotype contributing to vascular dysfunction.

Main Methods:

  • MVECs were generated by polyethylene glycol-induced fusion of EA.hy926 cells.
  • Cells were exposed to LDL, and analyses included biochemical assays for cholesterol, ELISA for cytokines, quantitative real-time PCR for gene expression, and DIA-LC-MS for secretome profiling.
  • Immunocytochemistry was used to assess tight junction protein localization.

Main Results:

  • MVECs exhibited enhanced intracellular cholesterol accumulation upon LDL exposure compared to TECs.
  • MVECs displayed elevated basal pro-inflammatory marker expression (IL1B, IL6, NFKB1) and amplified IL6/IL8 response to LDL.
  • MVECs showed reduced expression of antioxidant, barrier integrity (TJP1), and hemostatic (VWF) genes, with decreased secretion of vWF and EDN1, and altered ZO-1 distribution, indicating junctional destabilization.

Conclusions:

  • MVECs represent a distinct endothelial phenotype with increased lipid accumulation and sustained pro-inflammatory activation.
  • MVECs possess altered secretory signaling, reduced barrier integrity, and diminished hemostatic potential.
  • These characteristics suggest MVECs contribute to chronic endothelial dysfunction and vascular inflammation, particularly under hyperlipidemic conditions.