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Perturbing Endothelial Biomechanics via Connexin 43 Structural Disruption

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Published on: October 4, 2019

Endothelial gap junctions are down-regulated by arsenic trioxide.

Yusan Chou¹, Cheng-Ho Tsai, Kwo-Chang Ueng

¹Department of Internal Medicine, Mackay Memorial Hospital, Taipei, Taiwan.

European Journal of Pharmacology

|June 15, 2007

Summary

Arsenic trioxide (As(2)O(3)), an anti-cancer drug, was found to inhibit endothelial gap junctions in both cell cultures and rats. This drug reduces connexin43 (Cx43) expression and gap-junction communication, impacting vascular endothelium function.

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Area of Science:

Cardiovascular Biology
Cell Biology
Pharmacology

Background:

Endothelial gap junctions are crucial for vascular homeostasis.
Arsenic trioxide (As(2)O(3)) is an anti-cancer agent with potential vascular effects.
Understanding As(2)O(3)'s impact on endothelial function is vital for patient safety.

Purpose of the Study:

To investigate the effects of As(2)O(3) on endothelial gap junctions.
To evaluate the impact of As(2)O(3) on connexin43 (Cx43) expression and gap-junction communication.
To assess As(2)O(3)'s influence on endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) levels.

Main Methods:

Human aortic endothelial cells (HAEC) were treated with varying concentrations of As(2)O(3).
Expression of Cx43, eNOS, and NO levels were measured in vitro.
Male Sprague-Dawley rats received intravenous As(2)O(3) or saline for 4 weeks, with subsequent analysis of aortic endothelial gap junctions, eNOS, and NO.

Main Results:

As(2)O(3) reduced HAEC Cx43 transcripts, gap junctions, and gap-junction communication.
Protease inhibitors prevented the As(2)O(3)-induced decrease in Cx43 gap junctions.
In rats, As(2)O(3) decreased endothelial gap junctions (Cx37, Cx40, Cx43) but did not alter eNOS or NO levels.

Conclusions:

As(2)O(3) inhibits gap-junction communication in the vascular endothelium.
The reduction in Cx43 involves transcriptional down-regulation and increased degradation.
While As(2)O(3) affects endothelial cells and rat models, its impact on eNOS and NO differs between in vitro and in vivo settings.