Fractalkine and its receptor (CX3CR1) in patients with stable coronary artery disease and diabetes mellitus.
BACKGROUND
Fractalkine and its receptor CX3CR1 are associated with atherosclerosis. In vitro studies have shown increased expression of fractalkine in endothelial and vascular smooth muscle cells when stimulated with a high concentration of glucose. Increased serum levels of fractalkine have been shown in patients with type 2 diabetes mellitus (T2DM) and also in unstable coronary artery disease (CAD) patients. We investigated whether CAD patients with T2DM or metabolic syndrome have increased circulating and gene expression levels of fractalkine compared to CAD patients without these conditions.


METHODS
Serum levels of fractalkine were analyzed by the enzyme-linked immunosorbent assay (ELISA) method in 1001 patients with angiographically verified CAD, of which 200 had T2DM and 244 had metabolic syndrome. All patients were taking aspirin as an antithrombotic treatment. Gene expression of fractalkine and CX3CR1 in circulating leukocytes was explored in a subset of patients (n=168).


RESULTS
We found no significant difference in circulating levels of fractalkine in patients with T2DM [653 (556, 775) pg/mL] compared to patients without T2DM [646 (553, 761) pg/mL], p=0.50. There was also no difference between patients with and without metabolic syndrome (p=0.60). Fractalkine was not expressed in circulating leukocytes, and CX3CR1 was not expressed differently between any of the groups (p=0.13 and p=0.32, respectively). Smokers had lower fractalkine levels (p<0.001), and patients on angiotensin II receptor blockers had higher levels (p=0.047) compared to nonaffected patients.


CONCLUSIONS
In the present CAD population, no differences in circulating levels of fractalkine or expression levels of CX3CR1 were observed between patients with and without T2DM, or with and without metabolic syndrome, which may be related to their underlying disease.
Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevaal, Oslo, Norway. idaunh@ous-hf.no
Ida Unhammer
IU
Njerve
Alf Åge
AÅ
Pettersen
Trine Baur
TB
Opstad
Harald
H
Arnesen
Ingebjørg
I
Seljeflot
D000368:Aged; D000073883:CX3C Chemokine Receptor 1; D054428:Chemokine CX3CL1 / Q000097:blood* / Q000235:genetics* / Q000378:metabolism; D003324:Coronary Artery Disease / Q000097:blood / Q000150:complications / Q000235:genetics / Q000378:metabolism; D003924:Diabetes Mellitus, Type 2 / Q000097:blood / Q000150:complications / Q000235:genetics / Q000378:metabolism; D003925:Diabetic Angiopathies / Q000097:blood / Q000235:genetics / Q000378:metabolism; D018450:Disease Progression; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D015870:Gene Expression; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood / Q000235:genetics / Q000378:metabolism; D008875:Middle Aged; D016032:Randomized Controlled Trials as Topic; D019707:Receptors, Chemokine / Q000097:blood* / Q000235:genetics* / Q000378:metabolism
D000073883:CX3C Chemokine Receptor 1; C095235:CX3CR1 protein, human; D054428:Chemokine CX3CL1; D019707:Receptors, Chemokine