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Ethanol Enhances Endothelial Rigidity by Targeting VE-Cadherin-Implications for Acute Aortic Dissection.

Joscha Mulorz¹, Wiebke Ibing¹, Melanie Cappallo^1,2,3

¹Clinic for Vascular and Endovascular Surgery, Medical Faculty and University Hospital Duesseldorf, Heinrich-Heine-University, 40225 Duesseldorf, Germany.

Journal of Clinical Medicine

|August 12, 2023

Summary

This summary is machine-generated.

Established and potential risk factors like nicotine, angiotensin II, and ethanol exposure can increase endothelial rigidity in human aortic endothelial cells (hAoECs). This may lead to reduced cell deformability, potentially causing tears and acute aortic dissection (AAD).

Keywords:

acute aortic dissection cell adherence endothelial tear mechanical stability risk factors

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Published on: October 22, 2014

Area of Science:

Cardiovascular Biology
Endothelial Cell Function
Vascular Pathophysiology

Background:

Acute aortic dissection (AAD) is a life-threatening condition initiated by endothelial entry tears.
Hypertension and smoking are established risk factors, with excessive alcohol consumption emerging as a potential contributor.
The study investigates the impact of nicotine, angiotensin II, and ethanol on human aortic endothelial cells (hAoECs).

Purpose of the Study:

To investigate the effects of nicotine, angiotensin II, and ethanol on human aortic endothelial cell (hAoEC) function.
To explore potential mechanisms linking these risk factors to acute aortic dissection (AAD) development.
To assess changes in cell viability, adherence, migration, and junctional protein expression.

Main Methods:

Human aortic endothelial cells (hAoECs) were exposed to varying doses of nicotine, angiotensin II, and ethanol.
Cellular assays included scratch, live-cell imaging, WST-1 viability, in vitro vascular permeability, and hanging drop adherence.
Gene and protein expression of junctional complex proteins were analyzed via RT-qPCR, Western blotting, and immunohistochemistry.

Main Results:

Angiotensin II and ethanol exposure reduced metabolic viability in hAoECs.
Ethanol enhanced cell adherence, correlating with increased VE-cadherin expression.
Ethanol exposure decreased cell migration capacity, suggesting altered endothelial function.

Conclusions:

Nicotine, angiotensin II, and ethanol induce significant functional changes in hAoECs.
These substances may increase endothelial rigidity and reduce cell deformability.
This altered mechanical property could represent a novel mechanism contributing to endothelial entry tears in AAD.