Abstract 124: Association of AdipoR2 mRNA Expression on Peripheral Monocytes With Carotid Plaque Instability
Adiponectin, an adipose tissue secreted protein, possesses anti-atherosclerotic properties. Its effects are partly mediated through its action on monocytes, via receptors, AdipoR1 and AdipoR2. Circulating monocytes play a crucial role both in plaque initiation and in the progression of atherosclerosis. The aim of this ongoing study is to investigate for the first time whether there is differential expression of AdipoR1/AdipoR2 on human peripheral monocytes in patients with unstable vs. stable carotid atherosclerotic plaques.
Patients (n=20) with carotid stenosis of ≥50% scheduled for a carotid endarterectomy (CEA) were recruited from the Royal Victoria Hospital, Montreal, Canada. Blood samples were collected the morning of the CEA. A radioimmunoassay was used for plasma total adiponectin measurement. Circulating monocytes were isolated from mononuclear cells using a Magnetic Cell-Sorting technique with CD14+ Human Microbeads. Expression of AdipoR1/AdipoR2 mRNA on peripheral monocytes was determined using quantitative RT-PCR. Carotid plaque specimens were processed for histological analyses. Plaque instability was categorized according to the gold standard American Heart Association classification.
All specimens were graded as either a Type V (n=11) or a Type VI plaque (n=9). Type VI represents a more unstable lesion than Type V. AdipoR2 gene expression on monocytes was inversely associated with greater plaque instability; compared to patients with a Type V plaque, those with a Type VI plaque had 1.88-fold decreased AdipoR2 mRNA levels (p=0.046). AdipoR2 gene expression was found to be a trending predictor of a Type VI plaque (OR=2.93; 95% CI=0.87-9.81; p=0.082). AdipoR1 gene expression on monocytes did not differ between the two groups, while plasma adiponectin levels were lower in Type VI plaques (Type VI: 2.73 [2.19-3.96] μg/ml vs. Type V: 6.97 [4.69-10.07] μg/ml; p= 0.067). Plasma adiponectin levels did not correlate with the expression levels of AdipoR1/AdipoR2 on monocytes.
These results indicate that carotid plaque instability is associated with decreased AdipoR2 expression on peripheral monocytes. Our ongoing study may determine the underlying mechanisms linking adiponectin and its receptors with plaque instability.
Author Disclosures: K. Gasbarrino: None. H. Zheng: None. C. Mantzoros: None. C. Lai: None. J. Veinot: None. S. Daskalopoulou: None.
- © 2014 by American Heart Association, Inc.