© 2007 American Thoracic Society
Role of CD146 in Detection of Apoptotic Circulating Endothelial Cells in Obstructive Sleep ApneaTo the Editor:We read with interest the article by El Solh and colleagues, wherein the authors investigated endothelial cell apoptosis in patients with obstructive sleep apnea (OSA) in relation to vasomotor dysfunction and the effect of continuous positive airway pressure therapy (CPAP) on apoptotic circulating endothelial cells and vascular function (1). This is the first study in the literature describing a link between increased number of circulating apoptotic endothelial cells and impaired vascular function with the beneficial effect of CPAP treatment on endothelial cell apoptosis and endothelial dysfunction in patients with moderate OSA. In addition to limitations mentioned by authors, such as the limited number of patients, lack of detailed assessment of coronary artery disease, and duration of treatment, we would like to add an important criticism related to the detection of apoptotic endothelial cells using the CD146 endothelial marker, which merits further attention. CD146, also known as Mel-CAM, is a well-described specific adhesion marker of endothelial cells that has been reported in other cell lines including tumor, smooth muscle, dendritic, and stroma cells (2). Recently, its specificity as a marker of endothelial cell lineage was questioned by Elshal and coworkers (3), who reported that CD146 can no longer be regarded as an endothelium-specific marker, especially in the context of isolation of circulating endothelial cells, since it was also expressed on multiple lymphocyte subsets, implicating its role in adherence of T cells to the endothelium and their further activation. However, El Sohl and coworkers mention no coexpression of CD146 with B- and T-cell markers, although the same clone of anti-CD146 antibody was apparently used in both studies. Therefore, the detection of apoptotic lymphocyte subsets in parallel with endothelial cells cannot be excluded. With regard to the already known activation of T cells in patients with OSA (4, 5) and the tight regulation between activation and apoptosis in T-cell lineages (6), it is tempting to speculate that intermittent hypoxia, the hallmark of OSA, directly or via inflammatory cytokines not only activates endothelial cells and T lymphocytes but also orchestrates their programmed death. The latter could potentially result in immune derangement characterizing cardiovascular disorders. A controlled study investigating an association between apoptotic T cells and severity of OSA can provide us with useful pathogenetic insights and highlight novel therapeutic targets.
Medical School, Democritus University of Thrace, Alexandroupolis, Greece FOOTNOTES Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript. REFERENCES
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T cells in sleep apnea. Am J Respir Crit Care Med 2003;168:242–249.