Abstract
AimsThe tyrosine kinase receptor Axl is expressed in the vasculature, and growth arrest-specific protein 6 (Gas6) is its ligand. Plasma Gas6 levels have been shown to be associated with endothelial dysfunction markers and cardiovascular events. We set out to determine the plasma Gas6 levels in patients undergoing coronary artery bypass grafting (CABG) and investigate the expression of Gas6 and Axl in the aorta.Methods and ResultsImmunoassays were used to investigate plasma Gas6 levels in CABG patients (n = 19) and control subjects (n = 20). The expression of Gas6 and Axl in the injured aorta were examined by reverse transcription-polymerase chain reactions, real-time reverse transcription-polymerase chain reactions, western blotting, and immunohistochemical staining. Plasma Gas6 levels were significantly lower in CABG patients than in matched control subjects. In CABG patients, plasma Gas6 levels were negatively correlated with fasting glucose, E-selectin, and vascular cell adhesion molecule-1 levels. The levels predicted the operative mortality rate and were positively correlated with plasma soluble Axl (sAxl) levels and Gas6 expression in the aorta. Moreover, Gas6 expression was positively correlated with Axl expression in the aorta.ConclusionWe concluded that plasma Gas6 is associated with fasting glucose, endothelial dysfunction markers, sAxl values, and vascular Gas6 expression in CABG patients, and it predicts the operative mortality of these patients. These findings suggest that the Gas6/Axl system is crucial in vascular biology.
Highlights
Growth arrest-specific gene 6 (Gas6) was first described as one of the genes that was induced during growth arrest in serum-starved fibroblasts [1], but it was later shown to be widely expressed in various cell types, including vascular smooth muscle cells (VSMC), endothelial cells, and monocytes
The results showed that coronary artery bypass grafting (CABG) patients with high plasma growth arrest-specific protein 6 (Gas6) levels appeared to have lower fasting glucose, endothelial dysfunction markers, and predicted operative mortality rates
We first described that the plasma Gas6 and soluble Axl (sAxl) levels were significantly lower in CABG patients than in control subjects
Summary
Growth arrest-specific gene 6 (Gas6) was first described as one of the genes that was induced during growth arrest in serum-starved fibroblasts [1], but it was later shown to be widely expressed in various cell types, including vascular smooth muscle cells (VSMC), endothelial cells, and monocytes. Gas, which belongs to the family of plasma vitamin K-dependent proteins, shares 44% identity with anticoagulant protein S at the amino-acid level [2,3]. Despite some similarities in structure, Gas and protein S have different functional properties. Gas exerts its effects by binding the three members of the TYRO3, Axl, and Mer (TAM) family. Protein S is able to interact with TAM receptors, but in vitro studies have shown that it has an apparent lower affinity compared with Gas6 [4]. The Gas6/TAM system regulates an intriguing mix of processes that range from leukocyte sequestration and migration, platelet aggregation, and hematopoiesis to proliferation, apoptosis, and phagocytosis. The role of the Gas6/ TAM system has been perceived to be important in conditions of altered glucose tolerance, injury, inflammation, and repair [5]
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