Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Martin, Kevin B.; Stanchina, Michael; Kouttab, Nicola; Harrington, Elizabeth O.; Rounds, Sharon

doi:10.1007/s00408-008-9073-y

Cited by 50 publications

(43 citation statements)

References 29 publications

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“…The number of apoptotic endothelial cells in the circulation was lowered by therapy with nasal CPAP. However, contrasting results were reported in another recent study [92].…”

Section: Clinical Studiesmentioning

confidence: 56%

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Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

Taylor²,

2009

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There is increasing evidence that intermittent hypoxia plays a role in the development of cardiovascular risk in obstructive sleep apnoea syndrome (OSAS) through the activation of inflammatory pathways. The development of translational models of intermittent hypoxia has allowed investigation of its role in the activation of inflammatory mechanisms and promotion of cardiovascular disease in OSAS. There are noticeable differences in the response to intermittent hypoxia between body tissues but the hypoxia-sensitive transcription factors hypoxia-inducible factor-1 and nuclear factor-kB appear to play a key role in mediating the inflammatory and cardiovascular consequences of OSAS. Expanding our understanding of these pathways, the cross-talk between them and the activation of inflammatory mechanisms by intermittent hypoxia in OSAS will provide new avenues of therapeutic opportunity for the disease.

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“…The number of apoptotic endothelial cells in the circulation was lowered by therapy with nasal CPAP. However, contrasting results were reported in another recent study [92].…”

Section: Clinical Studiesmentioning

confidence: 56%

“…While lower numbers of EPCs have been noted in OSAS patients [93,94], one study has shown no statistical difference in either circulating endothelial cells or circulating EPCs in a group of OSAS patients, free of preexisting vascular disease, compared with age-and weightmatched controls [92].…”

Section: Clinical Studiesmentioning

confidence: 98%

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

Taylor²,

2009

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“…Lung homogenates were incubated with platelet-endothelial cell adhesion molecule (PECAM, CD31)-conjugated magnetic beads, and immunocomplexes were separated from homogenate with a magnetic column (25) and seeded on culture dishes in medium for 24 h. Cells were collected, and lysates were used for immunoblot analysis.…”

mentioning

confidence: 99%

Genetic disruption of protein kinase Cδ reduces endotoxin-induced lung injury

Chichger

Grinnell

Casserly

et al. 2012

American Journal of Physiology-Lung Cellular and Molecular Phys

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of acute lung injury and acute respiratory distress syndrome is characterized by sequestration of leukocytes in lung tissue, disruption of capillary integrity, and pulmonary edema. PKC␦ plays a critical role in RhoA-mediated endothelial barrier function and inflammatory responses. We used mice with genetic deletion of PKC␦ (PKC␦ Ϫ/Ϫ ) to assess the role of PKC␦ in susceptibility to LPS-induced lung injury and pulmonary edema. Under baseline conditions or in settings of increased capillary hydrostatic pressures, no differences were noted in the filtration coefficients (kf) or wet-to-dry weight ratios between PKC␦ ϩ/ϩ and PKC␦ Ϫ/Ϫ mice. However, at 24 h after exposure to LPS, the k f values were significantly higher in lungs isolated from PKC␦ ϩ/ϩ than PKC␦ Ϫ/Ϫ mice. In addition, bronchoalveolar lavage fluid obtained from LPS-exposed PKC␦ ϩ/ϩ mice displayed increased protein and cell content compared with LPS-exposed PKC␦ Ϫ/Ϫ mice, but similar changes in inflammatory cytokines were measured. Histology indicated elevated LPS-induced cellularity and inflammation within PKC␦ ϩ/ϩ mouse lung parenchyma relative to PKC␦ Ϫ/Ϫ mouse lungs. Transient overexpression of catalytically inactive PKC␦ cDNA in the endothelium significantly attenuated LPS-induced endothelial barrier dysfunction in vitro and increased kf lung values in PKC␦ ϩ/ϩ mice. However, transient overexpression of wild-type PKC␦ cDNA in PKC␦ Ϫ/Ϫ mouse lung vasculature did not alter the protective effects of PKC␦ deficiency against LPS-induced acute lung injury. We conclude that PKC␦ plays a role in the pathological progression of endotoxin-induced lung injury, likely mediated through modulation of inflammatory signaling and pulmonary vascular barrier function. endothelium; pulmonary edema; lipopolysaccharide; acute lung injury ACUTE RESPIRATORY DISTRESS syndrome (ARDS) is a major cause of morbidity and mortality in sepsis and severe pneumonia (26). Transudation of vascular fluid and protein from the pulmonary capillary lumen into the interstitium and alveolar air spaces impairs gas exchange, decreases lung compliance, and initiates a cascade of inflammatory events that leads to respiratory failure. This cascade is often characterized by sequestration of leukocytes in lung tissues, intravascular coagulation, and disruption of capillary integrity, leading to pulmonary edema (4).The vascular endothelium is a critical target for an endotoxin such as LPS, an established inflammatory and edemagenic agent. Circulating levels of LPS are elevated in patients with severe pneumonia or sepsis and can be used as a predictor of the development of ARDS (14).PKC␦ plays an important role in the maintenance of the lung vascular barrier. We observed enhanced endothelial barrier function following PKC␦ overexpression in vitro, effects that were mediated through the RhoA-GTPase pathway (21). We further noted that chemical and molecular inhibition in vivo and in vitro results in pulmonary edema formation and endothelial barrier dysfunction through reduced RhoA-GTPasemediated disrup...

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“…[11][12][13][14][15][16][17] Although they generally show abnormalities in the different aspects of endothelial function in OSA, the results show substantial variability, often with controversial findings. [11][12][13][14][15][16][17][18][19][20] This may be because of the concomitant confounding factors known to influence endothelial function independent of OSA. Also, myocardial blood flow reserve (MBFR) is a well-validated surrogate marker of coronary perfusion and provides an estimation of coronary flow reserve.…”

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confidence: 99%

Myocardial Perfusion by Myocardial Contrast Echocardiography and Endothelial Dysfunction in Obstructive Sleep Apnea

Butt

Khair²,

Dwivedi³

et al. 2011

Hypertension

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Abstract-Obstructive sleep apnea is associated with increased cardiovascular morbidity and mortality. We investigated myocardial perfusion using real-time quantitative myocardial contrast echocardiography with concurrent assessment of macrovascular and microvascular endothelial dysfunction in normotensive subjects with moderate-to-severe obstructive sleep apnea, who were compared with hypertensive and healthy subjects, as well as the impact of continuous positive airway pressure treatment on obstructive sleep apnea subjects. We measured flow (hyperemia)-mediated dilation and response to glyceryl trinitrate of brachial artery (ultrasound), cutaneous perfusion responses to acetylcholine and sodium nitroprusside (laser Doppler), pulse wave velocity, and circulating endothelial and endothelial progenitor cells in a total of 108 subjects (nϭ36 each of matched obstructive sleep apnea, hypertension, and healthy cohorts).

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Circulating Endothelial Cells and Endothelial Progenitor Cells in Obstructive Sleep Apnea

Cited by 50 publications

References 29 publications

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation

Genetic disruption of protein kinase Cδ reduces endotoxin-induced lung injury

Myocardial Perfusion by Myocardial Contrast Echocardiography and Endothelial Dysfunction in Obstructive Sleep Apnea

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