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Updated: May 29, 2025

Quantitation of Endothelial Cell Adhesiveness In Vitro
Published on: June 18, 2015
Fatty acid binding protein 3 activates endothelial adhesion of circulating monocytes and impairs endothelial
Yen-Wen Wu1,2,3, Jaw-Wen Chen2,4,5,6,7, Hao-Yuan Tsai1
1Division of Cardiology, Cardiovascular Medical Center, Far Eastern Memorial Hospital, New Taipei City, Taiwan.
Insights
Elevated fatty acid binding protein 3 (FABP3) is linked to coronary artery disease (CAD) and impairs blood vessel formation. This suggests FABP3 may be a therapeutic target for atherosclerosis.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pathophysiology
Background:
- Atherosclerotic cardiovascular diseases, including coronary artery disease (CAD), stem from vascular inflammation and endothelial dysfunction.
- Elevated fatty acid binding protein 3 (FABP3) is associated with cardiovascular diseases, but its precise role is not fully understood.
Purpose of the Study:
- To investigate the role of FABP3 in impaired angiogenesis.
- To elucidate the mechanisms by which FABP3 contributes to the development of atherosclerosis in CAD.
Main Methods:
- Clinical observational study of 1104 patients to analyze serum FABP3 and cardiovascular events.
- In vitro studies using primary cultured mononuclear cells, endothelial progenitor cells, and human coronary artery endothelial cells.
- In vivo studies in mice using matrigel plug neovascularization and aortic ring assays.
Main Results:
- Circulating FABP3 levels were higher in patients with cardiovascular events and CAD.
- FABP3 increased the expression of adhesion molecules in mononuclear cells and caused endothelial cell dysfunction via the ERK/p38/STAT1/VEGF pathway.
- FABP3 impaired angiogenesis in vivo and endothelial cell function under oxLDL or TNF-α stimulation.
Conclusions:
- FABP3 plays a significant role in the clinical and pathological aspects of atherosclerotic CAD.
- FABP3's impact on endothelial dysfunction and impaired angiogenesis highlights its potential as a therapeutic target for CAD.
Background And Purpose:
Vascular inflammation and endothelial dysfunction cause the development of atherosclerotic cardiovascular diseases including coronary artery disease (CAD). While elevated fatty acid binding protein 3 (FABP3) may be associated with the presence of cardiovascular diseases, its mechanistic effects remain unclear. This study aimed to investigate the role of FABP3 in impaired angiogenesis and the development of atherosclerosis in CAD.
Experimental Approach:
In total, 1104 patients were enrolled in a clinical observational study and the correlation between serum FABP3 and cardiovascular events were analysed. Another group of CAD patients and non-CAD subjects were enrolled, and their plasma FABP3 concentrations were measured. Primary cultured mononuclear cells endothelial progenitor cells and human coronary artery endothelial cells were used in vitro. Matrigel plug neovascularisation assay and the aortic ring assay were used in wild-type and apolipoprotein E-knockout mice in vivo.
Key Results:
Circulating FABP3 was up-regulated in the cardiovascular event-positive group and in the CAD patients. Mononuclear cells from the CAD patients presented increased expression of FABP3. FABP3 enhanced the expression of adhesion molecules, including integrin β2, integrin α4 and PSGL1 in mononuclear cells. FABP3 caused endothelial cell dysfunction through the ERK/p38/STAT1/VEGF signalling pathway. Moreover, oxLDL or TNF-α stimulations impaired endothelial cell function through FABP3-dependent signalling pathways. FABP3 also impaired in vivo angiogenesis.
Conclusion And Implications:
This study elucidates the clinical and pathological impact of FABP3 on atherosclerotic CAD. Future research may be necessary to evaluate whether FABP3 could be a therapeutic target, especially with regard to stable CAD.
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