Dataset Information

Altered in vitro endothelial repair and monocyte migration in obstructive sleep apnea: implication of VEGF and CRP.

ABSTRACT:

Study objectives

Although obstructive sleep apnea (OSA) causes cardiovascular morbidities through atherosclerosis induced by inflammation and endothelial dysfunction, OSA patients exhibit elevated plasma vascular endothelial growth factor (VEGF), which may represent an adaptive response to intermittent hypoxia. The aims of this study were to investigate whether in vitro endothelial wound healing and monocyte migration are affected by patient serum, and to determine the implication of circulating factors (VEGF and C-reactive protein).

Patients

Serum was collected from healthy controls (HC), "healthy" OSA, and metabolic syndrome (MS) patients with or without OSA.

Measurements and results

Along with the presence of OSA and/or MS, both VEGF and hsCRP were significantly elevated in patient serum. Their specific role was tested with blocking antibodies on primary endothelial cells for wound healing assay and on human monocytes for migration assay. Endothelial wound healing was reduced with OSA compared to HC serum, and even more significantly using MS+OSA patient serum. Altered wound healing with OSA serum was unmasked when blocking VEGF and restored when blocking CRP. Monocyte migration was activated with OSA serum, and further enhanced by MS+OSA patient serum. Blocking CRP in serum inhibited this migration.

Conclusions

Serum from OSA patient alters in vitro endothelial cell repair function and activates monocyte migration; this is further aggravated with the presence of metabolic syndrome. These effects are partly driven by VEGF and CRP, suggesting an unfavorable balance between the pro healing (VEGF) and pro injury (CRP) factors that may promote vascular injury in OSA with and without metabolic syndrome.

SUBMITTER: Briancon-Marjollet A

PROVIDER: S-EPMC4196066 | biostudies-literature | 2014 Nov

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Altered in vitro endothelial repair and monocyte migration in obstructive sleep apnea: implication of VEGF and CRP.

Briançon-Marjollet Anne A Henri Marion M Pépin Jean-Louis JL Lemarié Emeline E Lévy Patrick P Tamisier Renaud R

Sleep 20141101 11

<h4>Study objectives</h4>Although obstructive sleep apnea (OSA) causes cardiovascular morbidities through atherosclerosis induced by inflammation and endothelial dysfunction, OSA patients exhibit elevated plasma vascular endothelial growth factor (VEGF), which may represent an adaptive response to intermittent hypoxia. The aims of this study were to investigate whether in vitro endothelial wound healing and monocyte migration are affected by patient serum, and to determine the implication of cir ...[more]

PMID: 25364078

Similar Datasets

Project description:BackgroundObstructive sleep apnea (OSA) and inflammation are closely related. This study aimed to evaluate the associations and causal effect between C-reactive protein (CRP) and tumour necrosis factor-alpha (TNF-α) levels andOSA.MethodsPooled analysis was conducted to compare the expression differences of CRP and TNF-α between OSA patients with different severity and controls, and between continuous positive airway pressure (CPAP) and non-CPAP interventions for OSA patients. Using published GWAS summary statistics, we conducted a bidirectional two-sample Mendelian Randomization (MR) to estimate the causal relationships between CRP and TNF-α levels and OSA risk. Effect estimates were evaluated using inverse-variance weighted (IVW) as primary method, and several other MR methods as sensitivity analysis.ResultsBoth TNF-α (WMD [95%CI] = 5.86 [4.80-6.93] pg/ml, p < .00001) and CRP (WMD [95%CI] = 2.66 [2.15-3.17] mg/L, p < .00001), showed a significant increase in OSA patients compared with controls and this increasing trend was associated with OSA severity. Besides, compared to blank control (non-CPAP), CPAP treatment can reduce high TNF-α (WMD [95%CI]= -4.44 [-4.81, -4.07]pg/ml, p < .00001) and CRP (WMD [95%CI]= -0.91 [-1.65, -0.17] mg/l, p = .02) in OSA. Moreover, the primary MR analysis by IVW showed that OSA was the genetically predicted cause of elevated CRP (estimate: 0.095; 95% CI, [0.010-0.179]; p = .029) using six SNPs as the instrument variable, which were repeated by weighted median (estimate: 0.053; 95% CI, [0.007, 0.100]; p =.024) and MR RAPS (estimate: 0.109; 95% CI, [0.079, 0.140]; p = 1.98x10-12). Besides, the causal effect from elevated CRP on increased OSA risk was almost significant by IVW (OR:1.053; 95% CI, [1.000, 1.111]; p = .053). However, there were no causal associations between TNF-α and OSA from both directions.ConclusionsIncreased CRP and TNF-α were associated with OSA severity and sensible to CPAP treatment. Also, OSA had a suggestive causal effect on elevated CRP.

Dataset Information

Altered in vitro endothelial repair and monocyte migration in obstructive sleep apnea: implication of VEGF and CRP.

Study objectives

Patients

Measurements and results

Conclusions

Publications

Altered in vitro endothelial repair and monocyte migration in obstructive sleep apnea: implication of VEGF and CRP.

Similar Datasets

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