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High glucose induces human endothelial dysfunction through an Axl-dependent mechanism
Chien-Hsing Lee, Yi-Shing Shieh, Fone-Ching Hsiao
1Division of Endocrinology and Metabolism, Department of Internal Medicine, Tri-Service General Hospital, National Defense Medical Center, #325, Section 2, Cheng-Gong Rd,, Nei-Hu, Taipei, Taiwan. metahung@yahoo.com.
Cardiovascular Diabetology
|February 28, 2014
Summary
High glucose impairs endothelial function by altering the Gas6/Axl signaling pathway. Restoring Axl expression can reverse these negative effects, suggesting a therapeutic target for diabetic vascular disease.
Area of Science:
- Endocrinology
- Vascular Biology
- Cell Biology
Background:
- The Gas6/Axl signaling pathway plays a role in diabetic vascular complications.
- High glucose (HG) is implicated in endothelial dysfunction.
Purpose of the Study:
- To investigate the role of the Gas6/Axl system in high glucose-induced endothelial dysfunction.
Main Methods:
- Examined Axl signaling in human microvascular endothelial cells (HMEC-1) under various glucose concentrations.
- Assessed cell viability, tube formation, monocyte-endothelial cell adhesion, and molecular markers (ICAM-1, VCM-1, Akt, VEGF, VEGFR2).
Main Results:
- High glucose decreased Gas6/Axl expression and endothelial cell viability and tube formation, while increasing adhesion molecules.
- Axl restoration reversed HG-induced Akt phosphorylation, VCAM-1 expression, and endothelial dysfunction.
- Axl overexpression normalized VEGF and VEGFR2 expression in HG conditions.
- Diabetic patients showed reduced Axl and VEGFR2 expression in arteries.
Conclusions:
- High glucose alters Gas6/Axl signaling, impacting Akt and VEGF/VEGFR2 pathways.
- The Gas6/Axl system is implicated in high glucose-induced endothelial dysfunction.
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