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Annexin A1 expression in atherosclerotic carotid plaques and its relationship with plaque characteristics
1Division of Vascular Surgery, Department of Surgery, The University of Hong Kong Pokfulam Road, Hong Kong.
Objective:
Annexin A1, a calcium and phospholipid-binding protein, is an important endogenous modulator of inflammation. Whether this regulatory role extends to atherosclerosis is unknown. The aim of this study is to investigate the genetic and protein expression of Annexin A1 in carotid endarterectomy specimens from patients with significant carotid stenosis.
Materials And Methods:
The echogenicity of atherosclerotic plaques was determined by ultrasound prior to carotid endarterectomy (CEA) in 34 consecutively recruited patients with carotid stenosis exceeding 70%. The Annexin A1 messenger RNA and protein expression of the corresponding plaques obtained from those patients were analyzed by reverse transcriptase polymerase chain reaction (RT-PCR) and the immunohistochemical method respectively. Results were analyzed with respect to plaque characteristics and symptomatic disease.
Results:
There were 25 males and 9 females, with a mean age of 68.8. Ten patients were asymptomatic. The symptomatic patients' plaques were more echolucent (mean grey scale median (GSM) of 103) than those of asymptomatic patients (mean GSM = 126, p = 0.022). The Annexin A1 protein was constitutively expressed in all plaques, and Annexin A1 gene expression was statistically higher in patients with asymptomatic disease compared with those with neurological symptoms (87 ± 4% vs. 42 ± 6.2%; p < 0.001, unpaired t-test). The GSM score was positively correlated with Annexin A1 levels in patients with high-grade carotid artery stenosis (r = 0.501, p = 0.009).
Conclusions:
This is the first study to suggest that high Annexin A1 expression may have a stabilising effect in asymptomatic patients with less echolucent atherosclerotic plaques. Since atherosclerosis is an inflammatory process, we further postulate that Annexin A1 may play an essential role in preventing plaque complications or disease progression.
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