Статті в журналах: "Efflux Capacity"

1

Khera, Amit V., and Daniel J. Rader. "Cholesterol Efflux Capacity." Arteriosclerosis, Thrombosis, and Vascular Biology 33, no. 7 (July 2013): 1449–51. http://dx.doi.org/10.1161/atvbaha.113.301519.

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2

März, Winfried, and Andreas Ritsch. "Cholesterol Efflux Capacity." Journal of the American College of Cardiology 67, no. 21 (May 2016): 2488–91. http://dx.doi.org/10.1016/j.jacc.2016.04.005.

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3

Franssen, Remco, Alinda W. M. Schimmel, Sander I. van Leuven, Simone C. S. Wolfkamp, Erik S. G. Stroes, and Geesje M. Dallinga-Thie. "In Vivo Inflammation Does Not Impair ABCA1-Mediated Cholesterol Efflux Capacity of HDL." Cholesterol 2012 (April 24, 2012): 1–8. http://dx.doi.org/10.1155/2012/610741.

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HDL provides atheroprotection by facilitating cholesterol efflex from lipid-laden macrophages in the vessel wall. In vitro studies have suggested impaired efflux capacity of HDL following inflammatory changes. We assessed the impact of acute severe sepsis and mild chronic inflammatory disease on the efflux capacity of HDL. We hypothesize that a more severe inflammatory state leads to stronger impaired cholesterol efflux capacity. Using lipid-laden THP1 cells and fibroblasts we were able to show that efflux capacity of HDL from both patients with severe sepsis or with Crohn's disease (active or in remission), either isolated using density gradient ultracentrifugation or using apoB precipitation, was not impaired. Yet plasma levels of HDL cholesterol and apoA-I were markedly lower in patients with sepsis. Based on the current observations we conclude that inflammatory disease does not interfere with the capacity of HDL to mediate cholesterol efflux. Our findings do not lend support to the biological relevance of HDL function changes in vitro.

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4

Yano, Kouji, Ryunosuke Ohkawa, Megumi Sato, Akira Yoshimoto, Naoya Ichimura, Takahiro Kameda, Tetsuo Kubota, and Minoru Tozuka. "Cholesterol Efflux Capacity of Apolipoprotein A-I Varies with the Extent of Differentiation and Foam Cell Formation of THP-1 Cells." Journal of Lipids 2016 (2016): 1–9. http://dx.doi.org/10.1155/2016/9891316.

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Apolipoprotein A-I (apoA-I), the main protein component of high-density lipoprotein (HDL), has many protective functions against atherosclerosis, one of them being cholesterol efflux capacity. Although cholesterol efflux capacity measurement is suggested to be a key biomarker for evaluating the risk of development of atherosclerosis, the assay has not been optimized till date. This study aims at investigating the effect of different states of cells on the cholesterol efflux capacity. We also studied the effect of apoA-I modification by homocysteine, a risk factor for atherosclerosis, on cholesterol efflux capacity in different states of cells. The cholesterol efflux capacity of apoA-I was greatly influenced by the extent of differentiation of THP-1 cells and attenuated by excessive foam cell formation.N-Homocysteinylated apoA-I indicated a lower cholesterol efflux capacity than normal apoA-I in the optimized condition, whereas no significant difference was observed in the cholesterol efflux capacity between apoA-I in the excessive cell differentiation or foam cell formation states. These results suggest that cholesterol efflux capacity of apoA-I varies depending on the state of cells. Therefore, the cholesterol efflux assay should be performed using protocols optimized according to the objective of the experiment.

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5

Doonan, R. J., A. Hafiane, C. Lai, J. P. Veinot, J. Genest, and S. S. Daskalopoulou. "Cholesterol Efflux Capacity, Carotid Atherosclerosis, and Cerebrovascular Symptomatology." Arteriosclerosis, Thrombosis, and Vascular Biology 34, no. 4 (April 2014): 921–26. http://dx.doi.org/10.1161/atvbaha.113.302590.

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Objective— To investigate the association of cholesterol efflux capacity with carotid atherosclerosis and cerebrovascular disease. Approach and Results— Patients with high-grade carotid stenosis (n=154) were recruited from Vascular Surgery clinics and 9 healthy controls from the McGill University Health Network, Montreal, Canada. Cerebrovascular symptomatology history was obtained. Stenosis was assessed by carotid ultrasound. Fasting blood samples were collected and depleted of apolipoprotein B particles by polyethylene glycol precipitation from serum. Cholesterol efflux was determined by incubating apolipoprotein B–depleted serum in cAMP-stimulated J774 cells for 6 hours. Carotid specimens were classified by 2 vascular pathologists using the American Heart Association atheromatous plaque classification. Differences in efflux were assessed according to (1) stenosis, (2) American Heart Association classification, and (3) cerebrovascular symptomatology. Normalized efflux was significantly lower in patients with carotid atherosclerosis compared with controls (0.97±0.16 versus 1.5±0.46; P <0.0001). Efflux was inversely associated with stenosis; the odds ratio for 80% to 99% versus 50% to 79% stenosis of tertile 1 (lowest) versus tertile 3 (highest) of efflux was 3.78 (95% confidence interval, 1.18–12.06) after adjusting for age, sex, low-density lipoprotein, and high-density lipoprotein. There were significant differences in cholesterol efflux between American Heart Association fibroatheroma (Va, 0.91±0.13), mainly calcific (Vb, 0.97±0.15), and mainly fibrotic (Vc, 1.03±0.21; P =0.05). There were no significant differences in efflux according to symptomatology. Conclusions— Cholesterol efflux capacity is inversely associated with increasing carotid stenosis and is associated with more advanced carotid plaque morphology, suggesting that cholesterol efflux capacity may be a biomarker for severity of carotid atherosclerotic burden. Whether therapies targeting high-density lipoprotein quality could be useful for stabilizing carotid atherosclerosis needs to be assessed.

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6

Ma, Cheng-I. J., Jennifer A. Beckstead, Airlia Thompson, Anouar Hafiane, Rui Hao Leo Wang, Robert O. Ryan, and Robert S. Kiss. "Tweaking the cholesterol efflux capacity of reconstituted HDL." Biochemistry and Cell Biology 90, no. 5 (October 2012): 636–45. http://dx.doi.org/10.1139/o2012-015.

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Mechanisms to increase plasma high-density lipoprotein (HDL) or to promote egress of cholesterol from cholesterol-loaded cells (e.g., foam cells from atherosclerotic lesions) remain an important target to regress heart disease. Reconstituted HDL (rHDL) serves as a valuable vehicle to promote cellular cholesterol efflux in vitro and in vivo. rHDL were prepared with wild type apolipoprotein (apo) A-I and the rare variant, apoA-I Milano (M), and each apolipoprotein was reconstituted with phosphatidylcholine (PC) or sphingomyelin (SM). The four distinct rHDL generated were incubated with CHO cells, J774 macrophages, and BHK cells in cellular cholesterol efflux assays. In each cell type, apoA-I(M) SM-rHDL promoted the greatest cholesterol efflux. In BHK cells, the cholesterol efflux capacities of all four distinct rHDL were greatly enhanced by increased expression of ABCG1. Efflux to PC-containing rHDL was stimulated by transfection of a nonfunctional ABCA1 mutant (W590S), suggesting that binding to ABCA1 represents a competing interaction. This interpretation was confirmed by binding experiments. The data show that cholesterol efflux activity is dependent upon the apoA-I protein employed, as well as the phospholipid constituent of the rHDL. Future studies designed to optimize the efflux capacity of therapeutic rHDL may improve the value of this emerging intervention strategy.

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7

Dinnes, Donna Lee M., Stephen J. Nicholls, Wendy Jessup, and Leonard Kritharides. "HDL heterogeneity and serum efflux capacity." Current Opinion in Lipidology 26, no. 4 (August 2015): 350–52. http://dx.doi.org/10.1097/bor.0b013e32834b1fb1.

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8

Talbot, Charlotte P. J., Jogchum Plat, Andreas Ritsch, and Ronald P. Mensink. "Determinants of cholesterol efflux capacity in humans." Progress in Lipid Research 69 (January 2018): 21–32. http://dx.doi.org/10.1016/j.plipres.2017.12.001.

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9

Anastasius, Malcolm, Maaike Kockx, Wendy Jessup, David Sullivan, Kerry-Anne Rye, and Leonard Kritharides. "Cholesterol efflux capacity: An introduction for clinicians." American Heart Journal 180 (October 2016): 54–63. http://dx.doi.org/10.1016/j.ahj.2016.07.005.

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10

Rohatgi, Anand, and Scott M. Grundy. "Cholesterol Efflux Capacity as a Therapeutic Target." Journal of the American College of Cardiology 66, no. 20 (November 2015): 2211–13. http://dx.doi.org/10.1016/j.jacc.2015.09.012.

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11

Ritsch, A., A. Duerr, P. Kahler, T. Stojakovic, G. Silbernagel, H. Scharnagl, M. E. Kleber, and W. März. "HDL cholesterol efflux capacity and cardiovascular mortality." Atherosclerosis 241, no. 1 (July 2015): e28. http://dx.doi.org/10.1016/j.atherosclerosis.2015.04.106.

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12

Tavori, Hagai, Alexandra M. Fenton, Deanna L. Plubell, Sara Rosario, Elisabeth Yerkes, Rayna Gasik, Joshua Miles, et al. "Elevated Lipoprotein(a) Levels Lower ABCA1 Cholesterol Efflux Capacity." Journal of Clinical Endocrinology & Metabolism 104, no. 10 (April 9, 2019): 4793–803. http://dx.doi.org/10.1210/jc.2018-02708.

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Abstract Context Elevated serum lipoprotein(a) [Lp(a)] levels are associated with increased cardiovascular disease risk. ABCA1-mediated cholesterol efflux from macrophages may be an antiatherogenic process. Plasminogen (PLG) is a driver of ABCA1-mediated cholesterol efflux, and its action is inhibited by purified human Lp(a). Objective To determine the effects of Lp(a) in human serum on ABCA1 cholesterol efflux. Methods Cholesterol efflux capacity (CEC) was measured with two different cell-culture models using serum from 76 patients with either low (<50 mg/dL) or high (>50 mg/dL) Lp(a) levels. Results Using cAMP-stimulated J774 macrophages or baby hamster kidney fibroblasts overexpressing human ABCA1, we show that CEC was lower in patients with high Lp(a) levels compared with patients with low levels (−30.6%, P = 0.002 vs −24.1%, P < 0.001, respectively). Total-serum CEC negatively correlated with Lp(a) levels (r = −0.433, P = 0.0007 vs r = −0.505, P = 0.0011, respectively). These negative associations persisted after adjusting for serum cholesterol, age, sex, and statin use in a multiple linear regression model (adjusted R2 = 0.413 or 0.405, respectively) and were strengthened when further adjusting for the interaction between Lp(a) and PLG levels (adjusted R2 = 0.465 and 0.409, respectively). Total-serum and isolated Lp(a) from patients with high Lp(a) inhibited PLG-mediated ABCA1 cholesterol efflux. Conclusion Total-serum CEC is reduced in patients with high Lp(a) levels. This is in part due to the inhibition of PLG-mediated ABCA1 cholesterol efflux by Lp(a). Our findings suggest an atherogenic role for Lp(a) through its ability to inhibit CEC.

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13

Ke, Jing, Yan Wang, Simo Liu, Kun Li, YueChao Xu, Longyan Yang, and Dong Zhao. "Relationship of Para and Perirenal Fat and High-Density Lipoprotein and Its Function in Patients with Type 2 Diabetes Mellitus." International Journal of Endocrinology 2021 (December 22, 2021): 1–7. http://dx.doi.org/10.1155/2021/9286492.

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Background. Para and perirenal fat is a fat pad surrounding the kidneys. Recent studies showed the association between para and perirenal fat and cardiovascular diseases including atherosclerosis and hypertension. We aimed to assess the relationship between para-perirenal ultrasonographic fat thickness and serum high-density lipoprotein (HDL) level and cholesterol efflux capacity of HDL in patients with type 2 diabetes mellitus (T2DM). Methods. We recruited 58 subjects with T2DM and collected anthropometric indices including height, weight, waist circumference, and other clinical data. Para-perirenal ultrasonographic fat thickness (PUFT) was measured via ultrasound. Serum lipid profile and other metabolic indices were determined as well. Correlation analysis and regression analysis were performed to analyze the relationship between PUFT and HDL level and cholesterol efflux capacity in all patients and subgroups. Results. Patients with higher PUFT have lower serum HDL level but increased cholesterol efflux capacity. Further analysis showed that PUFT negatively correlated with the serum HDL level in all patients, with no difference in groups divided by body mass index (BMI). In addition, PUFT was positively correlated with cholesterol efflux capacity in all patients. Multiple stepwise regression analysis showed an independent association of PUFT and serum HDL level and cholesterol efflux capacity. Conclusions. PUFT is closely correlated with the serum HDL level and cholesterol efflux capacity in patients with T2DM.

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Enache, N., L. Laslo, M. Matei, M. Boboc, I. Cătuneanu, and G. Deák. "Analysis of the results from the applied technologies for carbon dioxide sampling in aquatic ecosystems." IOP Conference Series: Earth and Environmental Science 1216, no. 1 (July 1, 2023): 012006. http://dx.doi.org/10.1088/1755-1315/1216/1/012006.

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Abstract Globally, streams and rivers contain important stocks of carbon dioxide and release 1.8 ± 0.25 Pg of carbon each year. The literature review demonstrates that wetlands carbon sequestration capacity and effluxes are not homogenous. Considering those differences, it is crucial to comprehend how these effluxes vary depending on the characteristics of open water plots and areas with vegetation along river basins and how different weather conditions affect the variation of CO2 efflux. The purpose of this study was to analyse the various plots along Dambovita river’s watercourse in order to better understand the fluctuation of the CO2 efflux at the water-atmosphere interface and its dependent parameters. Here, we applied two complimentary methods with close chambers: dynamic by respiration chamber and static by injection kit in order to describe CO2 efflux data sets. Additionally, we measured simultaneously the weather parameters (air temperature, precipitation, wind speed), but also the water quality parameters. The CO2 efflux results are a starting point for improving the emission factor for rivers in temperate climate zone, which is 1.46 for default values at the country level. Also, the analysis performed contributes to a better understanding of how spatial and temporal variability of river characteristics impacts CO2 effluxes.

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15

Ritsch, Andreas, Angela Duerr, Patrick Kahler, Monika Hunjadi, Tatjana Stojakovic, Guenther Silbernagel, Hubert Scharnagl, Marcus E. Kleber, and Winfried März. "Cholesterol Efflux Capacity and Cardiovascular Disease: The Ludwigshafen Risk and Cardiovascular Health (LURIC) Study." Biomedicines 8, no. 11 (November 21, 2020): 524. http://dx.doi.org/10.3390/biomedicines8110524.

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(1) Background and Aims: Efforts to reduce coronary artery disease (CAD) by raising high-density lipoprotein (HDL) cholesterol (HDL-C) have not been uniformly successful. A more important factor than HDL-C may be cellular cholesterol efflux mediated by HDL, which has been shown to be associated with CAD. In this report, we analyzed the influence of cardiovascular biomarkers and risk factors on cholesterol efflux in a prospective observational study of patients referred to coronary angiography. (2) Methods: HDL-mediated efflux capacity was determined for 2468 participants of the Ludwigshafen Risk and Cardiovascular Health (LURIC) study who were referred to coronary angiography at baseline between 1997 and 2000. Median follow-up time was 9.9 years. Primary and secondary endpoints were cardiovascular and all-cause mortality, respectively. (3) Results: Cholesterol efflux strongly correlated with HDL-related markers including HDL cholesterol, HDL phospholipids, and apolipoproteins AI and AII, as well as HDL particle concentration, which was not seen for low density lipoprotein (LDL) markers including LDL cholesterol and apoB. Cholesterol efflux was associated negatively with C-reactive protein (CRP), fibrinogen, interleukin-6 (IL-6), and serum amyloid A. Cardiovascular mortality was higher in patients in the lowest cholesterol efflux quartile. This association was weakened, but not fully abolished, after adjustment for HDL cholesterol. (4) Conclusions: We demonstrate that cholesterol efflux was associated with HDL-composition as well as inflammatory burden in patients referred for coronary angiography, and that this inversely predicts cardiovascular mortality independently of HDL cholesterol.

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Holzer, Michael, Peter Wolf, Sanja Curcic, Ruth Birner-Gruenberger, Wolfgang Weger, Martin Inzinger, Dalia El-Gamal, Christian Wadsack, Akos Heinemann, and Gunther Marsche. "Psoriasis alters HDL composition and cholesterol efflux capacity." Journal of Lipid Research 53, no. 8 (May 30, 2012): 1618–24. http://dx.doi.org/10.1194/jlr.m027367.

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17

Brownell, Nicholas, and Anand Rohatgi. "Modulating cholesterol efflux capacity to improve cardiovascular disease." Current Opinion in Lipidology 27, no. 4 (August 2016): 398–407. http://dx.doi.org/10.1097/mol.0000000000000317.

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Rohatgi, Anand, Amit Khera, Jarett D. Berry, Edward G. Givens, Colby R. Ayers, Kyle E. Wedin, Ian J. Neeland, et al. "HDL Cholesterol Efflux Capacity and Incident Cardiovascular Events." New England Journal of Medicine 371, no. 25 (December 18, 2014): 2383–93. http://dx.doi.org/10.1056/nejmoa1409065.

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19

MOON, MARY ANN. "HDL Efflux Capacity May Correlate With CAD Risk." Family Practice News 41, no. 2 (February 2011): 22. http://dx.doi.org/10.1016/s0300-7073(11)70071-8.

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20

Holzer, Michael, Ruth Birner-Grünberger, Tatjana Stojaković, Dalia El-Gamal, Veronika Binder, Christian Wadsack, Ákos Heinemann, and Gunther Marsche. "Uremia alters HDL composition and cholesterol efflux capacity." BMC Pharmacology and Toxicology 13, Suppl 1 (2012): A15. http://dx.doi.org/10.1186/2050-6511-13-s1-a15.

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21

Ritsch, Andreas, Monika Hunjadi, Tatjana Stojakovic, Jürgen E. Scherberich, Günther Silbernagel, Hubert Scharnagl, Graciela E. Delgado, Marcus E. Kleber, and Winfried März. "Independent Effects of Kidney Function and Cholesterol Efflux on Cardiovascular Mortality." Biomedicines 10, no. 8 (July 29, 2022): 1832. http://dx.doi.org/10.3390/biomedicines10081832.

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Background: Impaired renal function is associated with cardiovascular and all-cause mortality. In the general population, HDL-cholesterol is associated with cardiovascular events, which is not true in patients with chronic kidney disease (CKD). This has been attributed to abnormal HDL function in CKD. Methods: In this study, we analyzed the association of genetic markers for kidney function with cholesterol efflux capacity as one of the major HDL functions, as well as with cardiovascular mortality, in 2469 patients of the Ludwigshafen Risk and Cardiovascular Health Study who all underwent coronary angiography. Results: A genetic score of 53 SNPs associated with GRF and the uromodulin SNP rs12917707 were inversely correlated with cholesterol efflux capacity. This was in line with the observed association between cholesterol efflux capacity and kidney function in these patients. Adjustment for eGFR and uromodulin as markers of kidney function did not affect the relationship between cholesterol efflux and cardiovascular mortality. Conclusions: Our data propose the view that cholesterol efflux and kidney function are exerting their effects on cardiovascular mortality via different and independent pathways. Decreased cholesterol efflux may therefore not mediate the effects of impaired kidney function on cardiovascular mortality.

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Yang, Bo, and Ceredwyn E. Hill. "Nifedipine modulation of biliary GSH and GSSG/ conjugate efflux in normal and regenerating rat liver." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 1 (July 1, 2001): G85—G94. http://dx.doi.org/10.1152/ajpgi.2001.281.1.g85.

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Canalicular glutathione secretion provides the major driving force for bile acid-independent bile flow (BAIF), although the pathways involved are not established. The hypothesis that GSH efflux proceeds by a route functionally distinct from the high-affinity, low-capacity, mrp2-mediated pathway was tested by using perfused rat liver and three choleretic compounds that modify biliary secretion of GSH (the dihydropyridine nifedipine and organic anion probenecid) or GSSG [sodium nitroprusside (SNP)]. Whereas nifedipine (30 μM) stimulated GSH secretion and blocked SNP-stimulated GSSG efflux and choleresis, SNP (1 mM) was ineffective against nifedipine-stimulated GSH efflux or BAIF, suggesting that most GSSG exits through a GSH-inhibitable path independent of high-affinity GSSG/glutathione conjugate transport. Three observations support this proposal. SNP, but not nifedipine, significantly inhibited bromosulfophthalein (BSP, 1 μM) excretion. Probenecid (1 mM) blocked resting or nifedipine-stimulated GSH secretion but only weakly inhibited BSP excretion. Glutathione, but not BSP, efflux capacity was reduced following partial hepatectomy. We suggest GSH efflux is mediated by a high-capacity organic anion pathway capable of GSSG transport when its high-affinity route is saturated.

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23

Liu, Xiaoran, Josephine Garban, Peter J. Jones, Jack Vanden Heuvel, Benoît Lamarche, David J. Jenkins, Philip W. Connelly, et al. "Diets Low in Saturated Fat with Different Unsaturated Fatty Acid Profiles Similarly Increase Serum-Mediated Cholesterol Efflux from THP-1 Macrophages in a Population with or at Risk for Metabolic Syndrome: The Canola Oil Multicenter Intervention Trial." Journal of Nutrition 148, no. 5 (May 1, 2018): 721–28. http://dx.doi.org/10.1093/jn/nxy040.

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Abstract Background Cholesterol efflux plays an important role in preventing atherosclerosis progression. Vegetable oils with varying unsaturated fatty acid profiles favorably affect multiple cardiovascular disease risk factors; however, their effects on cholesterol efflux remain unclear. Objective The objectives of this study were to examine the effects of diets low in saturated fatty acids (SFAs) with varying unsaturated fatty acid profiles on serum-mediated cholesterol efflux and its association with the plasma lipophilic index and central obesity. Methods The present study is a randomized, crossover, controlled-feeding study. Participants [men: n = 50; women: n = 51; mean ± SE age: 49.5 ± 1.2 y; body mass index (in kg/m2): 29.4 ± 0.4] at risk for or with metabolic syndrome (MetS) were randomly assigned to 5 isocaloric diets containing the treatment oils: canola oil, high oleic acid–canola oil, DHA-enriched high oleic acid–canola oil, corn oil and safflower oil blend, and flax oil and safflower oil blend. These treatment oils were incorporated into smoothies that participants consumed 2 times/d. For a 3000-kcal diet, 60 g of treatment oil was required to provide 18% of total energy per day. Each diet period was 4 wk followed by a 2- to 4-wk washout period. We quantified cholesterol efflux capacity with a validated ex vivo high-throughput cholesterol efflux assay. Statistical analyses were performed with the use of the SAS mixed-model procedure. Results The 5 diets increased serum-mediated cholesterol efflux capacity from THP-1 macrophages similarly by 39%, 34%, 55%, 49% and 51%, respectively, compared with baseline (P < 0.05 for all). Waist circumference and abdominal adiposity were negatively correlated with serum-mediated cholesterol efflux capacity (r = −0.25, P = 0.01, r = −0.33, P = 0.02, respectively). Conclusion Diets low in SFAs with different monounsaturated fatty acid and polyunsaturated fatty acid profiles improved serum-mediated cholesterol efflux capacity in individuals with or at risk for MetS. This mechanism may account, in part, for the cardiovascular disease benefits of diets low in SFAs and high in unsaturated fatty acids. Importantly, central obesity is inversely associated with cholesterol efflux capacity. This trial was registered at www.clinicaltrials.gov as NCT01351012.

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Norimatsu, Kenji, Takashi Kuwano, Shin-ichiro Miura, Tomohiko Shimizu, Yuhei Shiga, Yasunori Suematsu, Yuiko Miyase, et al. "Significance of the percentage of cholesterol efflux capacity and total cholesterol efflux capacity in patients with or without coronary artery disease." Heart and Vessels 32, no. 1 (April 22, 2016): 30–38. http://dx.doi.org/10.1007/s00380-016-0837-7.

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Huang, Jiansheng, Patricia G. Yancey, Huan Tao, Mark S. Borja, Loren E. Smith, Valentina Kon, Sean S. Davies, and MacRae F. Linton. "Reactive Dicarbonyl Scavenging Effectively Reduces MPO-Mediated Oxidation of HDL and Restores PON1 Activity." Nutrients 12, no. 7 (June 30, 2020): 1937. http://dx.doi.org/10.3390/nu12071937.

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Atheroprotective functions of high-density lipoproteins (HDL) are related to the activity of HDL-associated enzymes such as paraoxonase 1 (PON1). We examined the impact of inhibition of myeloperoxidase (MPO)-mediated HDL oxidation by PON1 on HDL malondialdehyde (MDA) content and HDL function. In the presence of PON1, crosslinking of apoAI in response to MPO-mediated oxidation of HDL was abolished, and MDA-HDL adduct levels were decreased. PON1 prevented the impaired cholesterol efflux capacity of MPO-oxidized HDL from Apoe−/− macrophages. Direct modification of HDL with MDA increased apoAI crosslinking and reduced the cholesterol efflux capacity. MDA modification of HDL reduced its anti-inflammatory function compared to native HDL. MDA-HDL also had impaired ability to increase PON1 activity. Importantly, HDL from subjects with familial hypercholesterolemia (FH-HDL) versus controls had increased MDA-apoAI adducts, and PON1 activity was also impaired in FH. Consistently, FH-HDL induced a pro-inflammatory response in Apoe−/− macrophages and had an impaired ability to promote cholesterol efflux. Interestingly, reactive dicarbonyl scavengers, including 2-hydroxybenzylamine (2-HOBA) and pentyl-pyridoxamine (PPM), effectively abolished MPO-mediated apoAI crosslinking, MDA adduct formation, and improved cholesterol efflux capacity. Treatment of hypercholesterolemic mice with reactive dicarbonyl scavengers reduced MDA-HDL adduct formation and increased HDL cholesterol efflux capacity, supporting the therapeutic potential of reactive carbonyl scavenging for improving HDL function.

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Stadler, Julia T., Harald Mangge, Alankrita Rani, Pero Curcic, Markus Herrmann, Florian Prüller, and Gunther Marsche. "Low HDL Cholesterol Efflux Capacity Indicates a Fatal Course of COVID-19." Antioxidants 11, no. 10 (September 21, 2022): 1858. http://dx.doi.org/10.3390/antiox11101858.

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Plasma membrane cholesterol is required for proper trafficking and localization of receptors that facilitate severe acute respiratory syndrome coronavirus 2 infection. High-density lipoproteins (HDL) mobilize plasma membrane cholesterol, and HDL-cholesterol levels are associated with the severity of COVID-19 disease and mortality. However, HDL-cholesterol levels poorly reflect the function of this complex family of particles, and a detailed assessment of COVID-19-associated changes in HDL functionality and its prognostic value is lacking. In the present study, we assessed HDL cholesterol efflux capacity, HDL anti-inflammatory and antioxidant properties, and changes in HDL composition and metabolism in COVID-19 (n = 48) and non-COVID pneumonia patients (n = 32). COVID-19 infection markedly reduced the activity of lecithin-cholesteryl-acyltransferase and functional parameters of HDL, such as the cholesterol efflux capacity, arylesterase activity of paraoxonase 1, and anti-oxidative capacity of apoB-depleted serum when compared to non-COVID pneumonia at baseline, paralleled by markedly reduced levels of HDL-cholesterol. Of particular interest, low HDL cholesterol efflux capacity was associated with increased mortality risk in COVID-19 patients, independent of HDL-C levels. Our results highlight profound effects of COVID-19 infection on HDL function, metabolism, and composition. Low HDL cholesterol efflux capacity indicates a fatal course of COVID-19, independent of HDL-cholesterol levels.

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Kudinov, V. A., T. S. Zakharova, T. I. Torkhovskaya, V. A. Kashirtseva, G. E. Morosevich, O. M. Ipatova, and A. I. Archakov. "Improving of HDL capacity for macrophages cholesterol efflux after plasma incubation with phospholipid nanoparticles." Biomeditsinskaya Khimiya 64, no. 3 (2018): 253–56. http://dx.doi.org/10.18097/pbmc20186403253.

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In connection with recent data about antiatherogenic importance of not only plasma HDL concentration, but of their cell cholesterol efflux capacity as well, the possibility of its correction by phospholipid (PL) nanoparticles was studied. Blood plasma was incubated with earlier elaborated PL nanoparticles emulsion with the particle diameter up to 30 nm, and HDL cholesterol efflux capacity of apo B-depleted plasma was studied. Using macrophages THP-1 preloaded 3H-cholesterol were used. The addition of incubated plasma supernatants with the elevated PL/apo A-1 ratio to cell media resulted in almost increase in two fold 3H-cholesterol efflux as compared with native HDL. The maximal efflux was observed at the PL/apo A-1 ratio of 1.06 as compared with native apo B-depleted plasma (the PL/apo A-1 ratio of 0.85). Results suggest possible usage of ultrasmall PL nanoparticles for regeneration of impaired antiatherogenic HDL functionality. This approach seems to be predominant compared with the usage of PL emulsions with detergent or apoprotein A1.

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28

Thomas, Michael J., and Mary G. Sorci-Thomas. "SAA: a link between cholesterol efflux capacity and inflammation?" Journal of Lipid Research 56, no. 8 (June 15, 2015): 1383–85. http://dx.doi.org/10.1194/jlr.c061366.

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29

Toth, P. P. "Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis." Yearbook of Endocrinology 2011 (January 2011): 63–66. http://dx.doi.org/10.1016/j.yend.2011.06.035.

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30

Khera, Amit V., Marina Cuchel, Margarita de la Llera-Moya, Amrith Rodrigues, Megan F. Burke, Kashif Jafri, Benjamin C. French, et al. "Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis." New England Journal of Medicine 364, no. 2 (January 13, 2011): 127–35. http://dx.doi.org/10.1056/nejmoa1001689.

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31

Holmes, David. "Cholesterol efflux capacity—inverse association with incident cardiovascular disease." Nature Reviews Endocrinology 11, no. 2 (December 9, 2014): 64. http://dx.doi.org/10.1038/nrendo.2014.217.

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32

Moneta, G. L. "Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis." Yearbook of Vascular Surgery 2011 (January 2011): 6–8. http://dx.doi.org/10.1016/j.yvas.2011.07.044.

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33

Stockman, J. A. "Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis." Yearbook of Pediatrics 2012 (January 2012): 206–8. http://dx.doi.org/10.1016/j.yped.2011.06.028.

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34

Koekemoer, A. L., V. Codd, N. Masca, M. Musameh, and N. J. Samani. "Large scale analysis of determinants of HDL efflux capacity." Atherosclerosis 237, no. 2 (December 2014): e10. http://dx.doi.org/10.1016/j.atherosclerosis.2014.10.061.

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35

Khera, A. V., M. Cuchel, and M. de la Llera-moya. "Cholesterol Efflux Capacity, High-Density Lipoprotein Function, and Atherosclerosis." Journal of Vascular Surgery 54, no. 1 (July 2011): 280–81. http://dx.doi.org/10.1016/j.jvs.2011.05.037.

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36

Duarte, João H. "Cholesterol efflux capacity—a new biomarker for cardiovascular risk?" Nature Reviews Cardiology 12, no. 1 (December 2, 2014): 2. http://dx.doi.org/10.1038/nrcardio.2014.198.

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37

Josefs, Tatjana, Debapriya Basu, Tomas Vaisar, Britt Arets, Jenny E. Kanter, Lesley-Ann Huggins, Yunying Hu, et al. "Atherosclerosis Regression and Cholesterol Efflux in Hypertriglyceridemic Mice." Circulation Research 128, no. 6 (March 19, 2021): 690–705. http://dx.doi.org/10.1161/circresaha.120.317458.

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Rationale: Hypertriglyceridemia and low HDL-C (high-density lipoprotein cholesterol), both of which are regulated by LpL (lipoprotein lipase) activity, associate with increased cardiovascular disease. Genetic regulators of LpL actions track with cardiovascular disease risk in humans. Whether this is due to changes in HDL-C or function or circulating triglyceride levels is unresolved. Objective: We created hypertriglyceridemia and HDL-C reduction in atherosclerotic mice to allow the assessment of how hypertriglyceridemia and reduced HDL-C affect regression of atherosclerosis and the phenotype of plaque macrophages. Methods and Results: Atherosclerosis regression was studied in control LpL floxed ( Lpl fl/fl ) mice and tamoxifen-inducible whole-body LpL knockout ( iLpl −/− ) mice with hypertriglyceridemia (≈500 mg/dL) and reduced HDL-C (≈50% reduction). Atherosclerosis regression was studied using 2 models in which advanced plaques resulting from hypercholesterolemia are exposed to normal LDL-C (low-density lipoprotein cholesterol) levels using aortic transplantation or treatments with oligonucleotides. In a subset of mice, we expressed hCETP (human cholesterol ester transfer protein) to humanize the relationship between apoB-lipoproteins and HDL. HDL particle number, cholesterol efflux capacity, and HDL proteome were measured in hypertriglyceridemia mice and humans. Surprisingly, hypertriglyceridemia and reduced HDL-C levels due to loss of LpL did not affect atherosclerosis lesion size or macrophage content (CD68+cells) in either model. Expression of hCETP and further reduction of HDL-C did not alter lesions. Sera from iLpl −/− mice had a decrease in total cholesterol efflux capacity, but not ABCA1 (ATP-binding cassette transporter A1)-mediated cholesterol efflux capacity. Hypertriglyceridemic humans, including those with LpL deficiency, had greater ABCA1-mediated cholesterol efflux capacity and total cholesterol efflux capacity per HDL particle number. Conclusions: Atherosclerosis regression in mice is driven by LDL-C reduction and is not affected by hypertriglyceridemia and plasma HDL-C levels.

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Stadler, Julia T., M. N. M. van Poppel, Christina Christoffersen, David Hill, Christian Wadsack, David Simmons, Gernot Desoye, and Gunther Marsche. "Gestational Hypertension and High-Density Lipoprotein Function: An Explorative Study in Overweight/Obese Women of the DALI Cohort." Antioxidants 12, no. 1 (December 29, 2022): 68. http://dx.doi.org/10.3390/antiox12010068.

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Gestational hypertension (GHTN) is associated with an increased cardiovascular risk for mothers and their offspring later in life. High-density lipoproteins (HDL) are anti-atherogenic by promoting efflux of cholesterol from macrophages and suppression of endothelial cell activation. Functional impairment of HDL in GHTN-complicated pregnancies may affect long-term health of both mothers and offspring. We studied functional parameters of maternal and neonatal HDL in 192 obese women (pre-pregnancy BMI ≥ 29), who were at high risk for GHTN. Maternal blood samples were collected longitudinally at <20 weeks, at 24–28 and 35–37 weeks of gestation. Venous cord blood was collected immediately after birth. Maternal and cord blood were used to determine functional parameters of HDL, such as HDL cholesterol efflux capacity, activity of the vaso-protective HDL-associated enzyme paraoxonase-1, and levels of the HDL-associated anti-inflammatory apolipoprotein (apo)M. In addition, we determined serum anti-oxidative capacity. Thirteen percent of the women were diagnosed with GHTN. While we found no changes in measures of HDL function in mothers with GHTN, we observed impaired HDL cholesterol efflux capacity and paraoxonase-1 activity in cord blood, while serum antioxidant capacity was increased. Of particular interest, increased maternal paraoxonase-1 activity and apoM levels in early pregnancy were associated with the risk of developing GHTN. GHTN significantly impairs HDL cholesterol efflux capacity as well as HDL PON1 activity in cord blood and could affect vascular health in offspring. Maternal paraoxonase-1 activity and apoM levels in early pregnancy associate with the risk of developing GHTN.

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39

Koehler, B., M. D. Corre, E. Veldkamp, and J. P. Sueta. "Chronic nitrogen addition causes a reduction in soil carbon dioxide efflux during the high stem-growth period in a tropical montane forest but no response from a tropical lowland forest in decadal scale." Biogeosciences Discussions 6, no. 5 (September 1, 2009): 8633–60. http://dx.doi.org/10.5194/bgd-6-8633-2009.

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Abstract. Atmospheric nitrogen (N) deposition is rapidly increasing in tropical regions. We studied the response of soil carbon dioxide CO2 efflux to long-term experimental N-addition (125 kg N ha−1 yr-1) in mature lowland and montane forests in Panamá. In the lowland forest, on soils with high nutrient-supplying and buffering capacity, fine litterfall and stem-growth were neither N- nor phosphorus-limited. In the montane forest, on soils with low nutrient supplying capacity and an organic layer, fine litterfall and stem-growth were N-limited. Our objectives were to 1) explore the influence of soil temperature and moisture on the dynamics of soil CO2 efflux and 2) determine the responses of soil CO2 efflux from an N-rich and N-limited forest to elevated N input. Annual soil CO2-C efflux was larger from the lowland (15.20±1.25 Mg C ha−1) than the montane forest (9.36±0.29 Mg C ha−1). In the lowland forest, soil moisture explained the largest fraction of the variance in soil CO2 efflux while soil temperature was the main explanatory variable in the montane forest. Soil CO2 efflux in the lowland forest did not differ between the control and 9–11 yr N-addition plots, suggesting that chronic N input to nutrient-rich tropical lowland forests on well-buffered soils may not change their C balance in decadal scale. In the montane forest, first year N addition did not affect soil CO2 efflux but annual CO2 efflux was reduced by 14% and 8% in the 2- and 3 yr N-addition plots, respectively, compared to the control. This reduction was caused by a decrease in soil CO2 efflux during the high stem-growth period of the year, suggesting a shift in carbon partitioning from below- to aboveground in the N-addition plots where stem diameter growth was promoted.

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40

Adorni, Maria Pia, Marta Biolo, Francesca Zimetti, Marcella Palumbo, Nicoletta Ronda, Paolo Scarinzi, Paolo Simioni, et al. "HDL Cholesterol Efflux and Serum Cholesterol Loading Capacity Alterations Associate to Macrophage Cholesterol Accumulation in FH Patients with Achilles Tendon Xanthoma." International Journal of Molecular Sciences 23, no. 15 (July 26, 2022): 8255. http://dx.doi.org/10.3390/ijms23158255.

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Achilles tendon xanthoma (ATX) formation involves macrophage cholesterol accumulation within the tendon, similar to that occurring in atheroma. Macrophage cholesterol homeostasis depends on serum lipoprotein functions, namely the high-density lipoprotein (HDL) capacity to promote cell cholesterol efflux (cholesterol efflux capacity, CEC) and the serum cholesterol loading capacity (CLC). We explored the HDL-CEC and serum CLC, comparing 16 FH patients with ATX to 29 FH patients without ATX. HDL-CEC through the main efflux mechanisms mediated by the transporters ATP binding cassette G1 (ABCG1) and A1 (ABCA1) and the aqueous diffusion (AD) process was determined by a cell-based radioisotopic technique and serum CLC fluorimetrically. Between the two groups, no significant differences were found in terms of plasma lipid profile. A trend toward reduction of cholesterol efflux via AD and a significant increase in ABCA1-mediated HDL-CEC (+18.6%) was observed in ATX compared to no ATX patients. In ATX-presenting patients, ABCG1-mediated HDL-CEC was lower (−11%) and serum CLC was higher (+14%) compared to patients without ATX. Considering all the patients together, ABCG1 HDL-CEC and serum CLC correlated with ATX thickness inversely (p = 0.013) and directly (p < 0.0001), respectively. In conclusion, lipoprotein dysfunctions seem to be involved in ATX physiopathology and progression in FH patients.

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41

Schachtl-Riess, J. F., C. Lamina, S. Schönherr, L. Forer, S. Coassin, G. Streiter, A. Kheirkhah, et al. "Genome-wide association study on HDL-mediated cholesterol efflux capacity." Atherosclerosis 355 (August 2022): 12. http://dx.doi.org/10.1016/j.atherosclerosis.2022.06.035.

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42

Silvain, Johanne, Mathieu Kerneis, Maryse Guerin, and Gilles Montalescot. "Modulation of cholesterol efflux capacity in patients with myocardial infarction." Current Opinion in Cardiology 34, no. 6 (November 2019): 714–20. http://dx.doi.org/10.1097/hco.0000000000000677.

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43

Kuusisto, Sanna, Michael V. Holmes, Pauli Ohukainen, Antti J. Kangas, Mari Karsikas, Mika Tiainen, Markus Perola, Veikko Salomaa, Johannes Kettunen, and Mika Ala-Korpela. "Direct Estimation of HDL-Mediated Cholesterol Efflux Capacity from Serum." Clinical Chemistry 65, no. 8 (August 1, 2019): 1042–50. http://dx.doi.org/10.1373/clinchem.2018.299222.

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Abstract BACKGROUND HDL-mediated cholesterol efflux capacity (HDL-CEC) is a functional attribute that may have a protective role in atherogenesis. However, the estimation of HDL-CEC is based on in vitro cell assays that are laborious and hamper large-scale phenotyping. METHODS Here, we present a cost-effective high-throughput nuclear magnetic resonance (NMR) spectroscopy method to estimate HDL-CEC directly from serum. We applied the new method in a population-based study of 7603 individuals including 574 who developed incident coronary heart disease (CHD) during 15 years of follow-up, making this the largest quantitative study for HDL-CEC. RESULTS As estimated by NMR-spectroscopy, a 1-SD higher HDL-CEC was associated with a lower risk of incident CHD (hazards ratio, 0.86; 95%CI, 0.79–0.93, adjusted for traditional risk factors and HDL-C). These findings are consistent with published associations based on in vitro cell assays. CONCLUSIONS These corroborative large-scale findings provide further support for a potential protective role of HDL-CEC in CHD and substantiate this new method and its future applications.

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44

Ye, Huiming, Guiyu Xu, Lihui Ren, and Jianjun Peng. "Cholesterol efflux capacity in coronary artery disease: a meta-analysis." Coronary Artery Disease 31, no. 7 (March 20, 2020): 642–49. http://dx.doi.org/10.1097/mca.0000000000000886.

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45

Vaisar, Tomáš, Chongren Tang, Ilona Babenko, Patrick Hutchins, Jake Wimberger, Anthony F. Suffredini, and Jay W. Heinecke. "Inflammatory remodeling of the HDL proteome impairs cholesterol efflux capacity." Journal of Lipid Research 56, no. 8 (May 20, 2015): 1519–30. http://dx.doi.org/10.1194/jlr.m059089.

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46

Hutchins, Patrick M., and Jay W. Heinecke. "Cholesterol efflux capacity, macrophage reverse cholesterol transport and cardioprotective HDL." Current Opinion in Lipidology 26, no. 5 (October 2015): 388–93. http://dx.doi.org/10.1097/mol.0000000000000209.

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47

Piemontese, A., S. Battista, C. Romain, F. Bernini, J. Cases, and I. Zanotti. "Cholesterol efflux capacity modulation by the nutraceutical compound “Oleactive®”." Nutrition, Metabolism and Cardiovascular Diseases 27, no. 1 (January 2017): e31-e32. http://dx.doi.org/10.1016/j.numecd.2016.11.087.

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48

Berrougui, H., I. Maxim, and A. Khalil. "Th-P15:228 Paraoxonase1 modulates HDL-mediated cholesterol efflux capacity." Atherosclerosis Supplements 7, no. 3 (January 2006): 543. http://dx.doi.org/10.1016/s1567-5688(06)82187-2.

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49

Favari, E., F. Zimetti, F. Bernini, M. Gomaraschi, S. Simonelli, L. Calabresi, M. Pirro, and G. Lupattelli. "In vivo acute systemic inflammation affects hdl cholesterol efflux capacity." Atherosclerosis 235, no. 2 (August 2014): e182. http://dx.doi.org/10.1016/j.atherosclerosis.2014.05.530.

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50

Chua, N. Y. C., R. Najme Khir, E. A. Rahman, C. Wen Lim, K. Shafiq Ibrahim, R. Ezman, J. Rizwal Ismail, and S. Kasim. "Cholesterol efflux capacity in young acute coronary syndrome in Malaysia." Atherosclerosis 275 (August 2018): e169-e170. http://dx.doi.org/10.1016/j.atherosclerosis.2018.06.512.

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