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Updated: Jul 16, 2026

Using En Face Immunofluorescence Staining to Observe Vascular Endothelial Cells Directly

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Lipid-Induced Endothelial Dysfunction: Pro-Atherogenic Properties of Multinucleated Variant Endothelial Cells.

Vadim Cherednichenko¹, Diana Kiseleva^1,2, Ulyana Khovantseva^1,3

¹Petrovsky National Research Center of Surgery, 119435 Moscow, Russia.

International Journal of Molecular Sciences

|July 15, 2026

Summary

Multinucleated variant endothelial cells (MVECs) show impaired barrier function and increased inflammation, contributing to cardiovascular disease development. These cells accumulate cholesterol and promote macrophage migration, highlighting their role in endothelial dysfunction.

Keywords:

atherosclerosis cholesterol accumulation endothelial barrier function endothelial dysfunction interleukin-6 interleukin-8 low-density lipoproteins multinucleated variant endothelial cells secretome proteomics transendothelial macrophage migration

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Published on: August 12, 2025

Area of Science:

Cardiovascular Biology
Endothelial Cell Biology
Molecular Medicine

Background:

Endothelial dysfunction is a key early event in cardiovascular diseases.
Multinucleated variant endothelial cells (MVECs) exist in the vascular wall, but their function is unclear.
Understanding MVEC function is crucial for elucidating endothelial dysfunction mechanisms.

Purpose of the Study:

To investigate the molecular and functional characteristics of MVECs.
To determine the contribution of MVECs to endothelial dysfunction.
To compare MVEC behavior with typical endothelial cells (TECs).

Main Methods:

Generated MVECs from human umbilical vein endothelial cells (HUVECs) via polyethylene glycol-induced fusion.
Exposed cells to low-density lipoproteins (LDL).
Performed transcriptomic and proteomic profiling, and functional assays (LDL transport, cholesterol accumulation, macrophage migration, cytokine secretion).

Main Results:

MVECs displayed altered signaling pathways, including reduced NF-κB pathway enrichment and impaired cytoskeletal organization.
MVECs showed increased intracellular cholesterol accumulation and enhanced macrophage migration.
MVECs exhibited a pro-inflammatory phenotype with elevated IL-6 and IL-8 secretion.

Conclusions:

MVECs represent a distinct endothelial cell phenotype with impaired barrier function, dysregulated lipid metabolism, and heightened inflammatory activity.
Accumulation of MVECs in the vascular wall may promote pro-atherogenic environments.
MVECs play a significant role in the initiation and progression of endothelial dysfunction.