Altered<i>in vitro</i>Endothelial Repair and Monocyte Migration in Obstructive Sleep Apnea: Implication of VEGF and CRP

Briançon‐Marjollet, Anne; Henri, Marion; Pépin, Jean‐Louis; Lemarié, Emeline; Lévy, Patrick; Tamisier, Renaud

doi:10.5665/sleep.4180

Cited by 23 publications

(24 citation statements)

References 33 publications

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“…We explored the effects of OSA during CPAP withdrawal on ADM, ET‐1 and VEGF, which are activated via HIF during hypoxic conditions. Cohort studies have suggested that these blood proteins play a role in cardiovascular disease in OSA . We found no increases in these markers during CPAP withdrawal.…”

Section: Discussioncontrasting

confidence: 69%

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Effect of OSA on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomized control trials

et al. 2016

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Section: Discussioncontrasting

confidence: 69%

“…Counter intuitively the increased ADM levels found in OSA have been proposed as an adaptive mechanism protective against cardiovascular disease . The effects of OSA on vascular endothelial growth factor (VEGF), an angiogenesis stimulator, are not clear …”

Section: Introductionmentioning

confidence: 99%

Effect of OSA on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomized control trials

et al. 2016

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“…Similar to our results, Dyugovskaya et al 2002 isolated mononuclear cells from OSA and healthy patients and found increased monocyte adhesion to cultured endothelial cells [54]. Other studies examined monocyte migration following OSA serum incubation and found significant monocyte migration in patients with both moderate and severe AHI [55]. Apneic serum also demonstrated a significant increase in mesenchymal stem cell chemotaxis [56].…”

Section: Discussionsupporting

confidence: 87%

Serum from obstructive sleep apnea patients induces inflammatory responses in coronary artery endothelial cells

et al. 2016

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Background and aims Obstructive sleep apnea (OSA) is characterized by intermittent airway obstruction and systemic hypoxia during sleep, which can contribute to an increase in reactive oxygen species, vascular remodeling, vasoconstriction and ultimately cardiovascular disease. Continuous positive airway pressure (CPAP) is a clinical therapy that maintains airway patency and mitigates several symptoms of OSA. However, it is currently unknown whether CPAP therapy also reduces the overall inflammatory potential in the circulation; to address this in an unbiased manner, we applied a novel endothelial biosensor approach, the serum cumulative inflammatory potential (SCIP) assay. Methods We studied healthy controls (n=7), OSA subjects receiving no treatment, (OSA controls) (n=7) and OSA subjects receiving CPAP for 3 months (n=8). Serum was obtained from OSA subjects before and after CPAP or no treatment. A battery of quantitative and functional assays was performed to assess the serum inflammatory potential, in terms of endothelial responses. For the SCIP assay, human coronary artery endothelial cells (hCAECs) were incubated with 5% serum in media from individual subjects for 4 h. qPCR was performed to assess endothelial inflammatory transcript (ICAM-1, VCAM-1, IL-8, P-selectin, CCL5, and CXCL12) responses to serum. Additionally, transendothelial resistance was measured in serum-incubated hCAECs following leukocyte challenge. Results hCAECs exhibited significant increases in VCAM-1, ICAM-1, IL-8 and P-selectin mRNA when incubated with serum from OSA patients compared to serum from healthy control subjects. Furthermore, compared to no treatment, serum from CPAP-treated individuals was less potent at inducing inflammatory gene expression in the SCIP assay. Similarly, in a leukocyte adhesion assay, naïve cells treated with serum from patients who received CPAP exhibited improved endothelial barrier function than cells treated with OSA control serum. Conclusions OSA results in greater serum inflammatory potential, thereby driving endothelial activation and dysfunction.

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“…However, given the weak correlations ( r = 0.24–0.25), these factors are not likely to fully explain the observed differences in endothelial migration in our study. Other circulating factors previously shown to be unfavorably altered in individuals with MetS include plasma insulin, endothelin‐1, plasminogen activator inhibitor‐1, nitric oxide, C‐reactive protein, and interleukin‐6 (Briançon‐Marjollet et al ; Chedraui et al ; Ahirwar et al ). Future studies should seek to determine the specific circulating factors potentially contributing to impaired endothelial migration with MetS.…”

Section: Discussionmentioning

confidence: 99%

Circulating microRNAs and endothelial cell migration rate are associated with metabolic syndrome and fitness level in postmenopausal African American women

et al. 2019

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Postmenopausal African American women are at elevated risk for metabolic syndrome (MetS), which predisposes them to cardiovascular disease and other chronic diseases. Circulating microRNAs (ci‐miR) are potential mediators of cardiometabolic diseases also impacted by cardiorespiratory fitness (CRF) level. Using real‐time quantitative PCR, we compared the expression of vascular‐related ci‐miRs (miR‐21‐5p, miR‐92a‐3p, miR‐126‐5p, miR‐146a‐5p, miR‐150‐5p, miR‐221‐3p) in sedentary, overweight/obese, postmenopausal African American women based on 1) presence ( n = 31) or absence ( n = 42) of MetS and 2) CRF level (VO 2peak ) (Very Low < 18.0 mL·kg −1 ·min −1 [ n = 31], Low = 18.0–22.0 mL·kg −1 ·min −1 [ n = 24], or Moderate >22.0 mL·kg −1 ·min −1 [ n = 18]). Endothelial migration rate in response to subjects’ serum was assessed to determine the effect of circulating blood‐borne factors on endothelial repair. Ci‐miR‐21‐5p was the only ci‐miR that differed between women with MetS compared to those without MetS (0.93 ± 0.43 vs. 1.28 ± 0.71, P = 0.03). There were borderline significant differences ( P = 0.06–0.09) in ci‐miR‐21‐5p, 126‐5p, and 221‐3p levels between the CRF groups, and these three ci‐miRs correlated with VO 2peak ( r = −0.25 to −0.28, P < 0.05). Endothelial migration rate was impaired in response to serum from women with MetS compared to those without after 16–24 h. Serum from women with Moderate CRF induced greater endothelial migration than the Very Low and Low CRF groups after 4 and 16–24 h, that was also not different from a young, healthy reference group. Ci‐miR‐21‐5p is lower in postmenopausal African American women with MetS, while ci‐miRs‐21‐5p, 126‐5p, and 221‐3p are associated with CRF. Factors which impair endothelial cell migration rate are present in serum of women with MetS, though having Moderate CRF may be protective.

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Alteredin vitroEndothelial Repair and Monocyte Migration in Obstructive Sleep Apnea: Implication of VEGF and CRP

Cited by 23 publications

References 33 publications

Effect of OSA on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomized control trials

Effect of OSA on hypoxic and inflammatory markers during CPAP withdrawal: Further evidence from three randomized control trials

Serum from obstructive sleep apnea patients induces inflammatory responses in coronary artery endothelial cells

Circulating microRNAs and endothelial cell migration rate are associated with metabolic syndrome and fitness level in postmenopausal African American women

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