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Original Research |

Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 Modulates Endothelial Apoptosis in Obstructive Sleep ApneaApoptosis in Obstructive Sleep Apnea

Morohunfolu E. Akinnusi, MD; Rachel Laporta, MA; Ali A. El-Solh, MD, MPH
Author and Funding Information

From the Veterans Affairs Western New York Healthcare System (Drs Akinnusi and El-Solh and Ms Laporta), Western New York Respiratory Research Center; and the Division of Pulmonary, Critical Care, and Sleep Medicine (Drs Akinnusi and El-Solh), Department of Medicine, and the Department of Social and Preventive Medicine (Dr El-Solh), University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY.

Correspondence to: Ali A. El-Solh, MD, MPH, Division of Pulmonary, Critical Care, and Sleep Medicine, Veterans Affairs Western New York Healthcare System, 3495 Bailey Ave, Buffalo, NY 14215-1199; e-mail: solh@buffalo.edu

Data are presented as mean ± SD. AHI = apnea-hypopnea index; OSA = obstructive sleep apnea; Spo2 = oxygen saturation by pulse oximeter.

Data are presented as mean ± SD. CPAP = continuous positive airway pressure. See Table 1 legend for expansion of other abbreviations.

CEC = circulating endothelial cell; eLOX-1 = endothelial lectin-like oxidized low-density lipoprotein receptor 1; SaO2 = oxygen saturation. See Table 1 legend for expansion of other abbreviations.

BMI was excluded from the analysis due to collinearity. See Table 1 and 3 legends for expansion of abbreviations.

For editorial comment see page 1400

Funding/Support: This study was supported by the American Academy of Sleep Medicine Physician-Scientist Training Award grant (M. E. A.) and the US Department of Veterans Affairs Merit Review Award [HSR&D 10-087-1 (A. A. E.-S.)].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


For editorial comment see page 1400

For editorial comment see page 1400

Funding/Support: This study was supported by the American Academy of Sleep Medicine Physician-Scientist Training Award grant (M. E. A.) and the US Department of Veterans Affairs Merit Review Award [HSR&D 10-087-1 (A. A. E.-S.)].

Funding/Support: This study was supported by the American Academy of Sleep Medicine Physician-Scientist Training Award grant (M. E. A.) and the US Department of Veterans Affairs Merit Review Award [HSR&D 10-087-1 (A. A. E.-S.)].

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


Chest. 2011;140(6):1503-1510. doi:10.1378/chest.11-0302
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Background:  Lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) is the major receptor for oxidized low-density lipoprotein in endothelial cells, and its expression is enhanced in proatherogenic settings. The objective of this study was to investigate the association between LOX-1 in freshly harvested human venous endothelial cells and apoptotic circulating endothelial cells in patients with obstructive sleep apnea (OSA).

Methods:  We conducted a prospective, interventional study of 38 patients with newly diagnosed OSA free of disease and 12 healthy control subjects. Plasma LOX-1 (pLOX-1) levels were measured using a commercially available enzyme-linked immunosorbent assay. Protein expression of LOX-1 was quantified by immunofluorescence in freshly harvested venous endothelial cells before and after 8 weeks of continuous positive airway pressure (CPAP) therapy. Circulating apoptotic endothelial cells (CD146+, CD45, and CD311) were assessed concomitantly by flow cytometry.

Results:  pLOX-1 levels were higher in subjects with OSA than in control subjects (326.9 ± 267.1 pg/mL and 141.1 ± 138.6 g/mL, respectively; P = .004). Patients with OSA showed a threefold increase in baseline endothelial expression of LOX-1 relative to control subjects. CPAP therapy resulted in a significant decrease in endothelial LOX-1 expression only in CPAP-adherent patients. Circulating apoptotic endothelial cells correlated directly with baseline expression of LOX-1 (R2 = 0.32, P = .01) after adjustment for age, BMI, and waist to hip ratio.

Conclusions:  Increased expression of LOX-1 in vivo is associated with endothelial apoptosis. Adherence to CPAP therapy may reverse these derangements.

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