LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection
Subnormal HDL-cholesterol (HDL-C) and apolipoprotein (apo)AI levels are characteristic of familial hypercholesterolemia (FH), reflecting perturbed intravascular metabolism with compositional anomalies in HDL particles, including apoE enrichment. Does LDL-apheresis, which reduces HDL-cholesterol, apo...
| Main Authors: | , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2011-12-01
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| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520408351 |
| _version_ | 1831678401833861120 |
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| author | Alexina Orsoni Samir Saheb Johannes H.M. Levels Geesje Dallinga-Thie Marielle Atassi Randa Bittar Paul Robillard Eric Bruckert Anatol Kontush Alain Carrié M. John Chapman |
| author_facet | Alexina Orsoni Samir Saheb Johannes H.M. Levels Geesje Dallinga-Thie Marielle Atassi Randa Bittar Paul Robillard Eric Bruckert Anatol Kontush Alain Carrié M. John Chapman |
| author_sort | Alexina Orsoni |
| collection | DOAJ |
| description | Subnormal HDL-cholesterol (HDL-C) and apolipoprotein (apo)AI levels are characteristic of familial hypercholesterolemia (FH), reflecting perturbed intravascular metabolism with compositional anomalies in HDL particles, including apoE enrichment. Does LDL-apheresis, which reduces HDL-cholesterol, apoAI, and apoE by adsorption, induce selective changes in HDL subpopulations, with relevance to atheroprotection? Five HDL subpopulations were fractionated from pre- and post-LDL-apheresis plasmas of normotriglyceridemic FH subjects (n = 11) on regular LDL-apheresis (>2 years). Apheresis lowered both plasma apoE (−62%) and apoAI (−16%) levels, with preferential, genotype-independent reduction in apoE. The mass ratio of HDL2:HDL3 was lowered from ∼1:1 to 0.72:1 by apheresis, reflecting selective removal of HDL2 mass (80% of total HDL adsorbed). Pre-LDL-apheresis, HDL2 subpopulations were markedly enriched in apoE, consistent with ∼1 copy of apoE per 4 HDL particles. Large amounts (50-66%) of apoE-HDL were removed by apheresis, preferentially in the HDL2b subfraction (−50%); minor absolute amounts of apoE-HDL were removed from HDL3 subfractions. Furthermore, pre-β1-HDL particle levels were subnormal following removal (−53%) upon apheresis, suggesting that cellular cholesterol efflux may be defective in the immediate postapheresis period. In LDL-receptor (LDL-R) deficiency, LDL-apheresis may enhance flux through the reverse cholesterol transport pathway and equally attenuate potential biglycan-mediated deposition of apoE-HDL in the arterial matrix. |
| first_indexed | 2024-12-20T04:59:07Z |
| format | Article |
| id | doaj.art-48a81323fae341548899f14a6d53d6e1 |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-20T04:59:07Z |
| publishDate | 2011-12-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-48a81323fae341548899f14a6d53d6e12022-12-21T19:52:38ZengElsevierJournal of Lipid Research0022-22752011-12-01521223042313LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotectionAlexina Orsoni0Samir Saheb1Johannes H.M. Levels2Geesje Dallinga-Thie3Marielle Atassi4Randa Bittar5Paul Robillard6Eric Bruckert7Anatol Kontush8Alain Carrié9M. John Chapman10INSERM UMR-S939, Hôpital de la Pitié-Salpetriere, Paris, France; Université Pierre et Marie Curie-Paris 6, Hôpital de la Pitié-Salpetriere, Paris, FranceHaemobiotherapy Unit, AP-HP, Hôpital de la Pitié-Salpetriere, Paris, FranceExperimental Vascular Medicine, Academic Medical Center, Amsterdam, The NetherlandsExperimental Vascular Medicine, Academic Medical Center, Amsterdam, The NetherlandsHaemobiotherapy Unit, AP-HP, Hôpital de la Pitié-Salpetriere, Paris, FranceMetabolic Biochemistry, AP-HP, Hôpital de la Pitié-Salpetriere, Paris, FranceINSERM UMR-S939, Hôpital de la Pitié-Salpetriere, Paris, France; Université Pierre et Marie Curie-Paris 6, Hôpital de la Pitié-Salpetriere, Paris, FranceEndocrinology-Metabolism Service, AP-HP, Hôpital de la Pitié-Salpetriere, Paris, FranceINSERM UMR-S939, Hôpital de la Pitié-Salpetriere, Paris, France; Université Pierre et Marie Curie-Paris 6, Hôpital de la Pitié-Salpetriere, Paris, FranceINSERM UMR-S939, Hôpital de la Pitié-Salpetriere, Paris, France; Université Pierre et Marie Curie-Paris 6, Hôpital de la Pitié-Salpetriere, Paris, France; Molecular and Oncologic Endocrinology, AP-HP, Hôpital de la Pitié-Salpetriere, Paris, France; andTo whom correspondence should be addressed.; INSERM UMR-S939, Hôpital de la Pitié-Salpetriere, Paris, France; Université Pierre et Marie Curie-Paris 6, Hôpital de la Pitié-Salpetriere, Paris, France; To whom correspondence should be addressed.Subnormal HDL-cholesterol (HDL-C) and apolipoprotein (apo)AI levels are characteristic of familial hypercholesterolemia (FH), reflecting perturbed intravascular metabolism with compositional anomalies in HDL particles, including apoE enrichment. Does LDL-apheresis, which reduces HDL-cholesterol, apoAI, and apoE by adsorption, induce selective changes in HDL subpopulations, with relevance to atheroprotection? Five HDL subpopulations were fractionated from pre- and post-LDL-apheresis plasmas of normotriglyceridemic FH subjects (n = 11) on regular LDL-apheresis (>2 years). Apheresis lowered both plasma apoE (−62%) and apoAI (−16%) levels, with preferential, genotype-independent reduction in apoE. The mass ratio of HDL2:HDL3 was lowered from ∼1:1 to 0.72:1 by apheresis, reflecting selective removal of HDL2 mass (80% of total HDL adsorbed). Pre-LDL-apheresis, HDL2 subpopulations were markedly enriched in apoE, consistent with ∼1 copy of apoE per 4 HDL particles. Large amounts (50-66%) of apoE-HDL were removed by apheresis, preferentially in the HDL2b subfraction (−50%); minor absolute amounts of apoE-HDL were removed from HDL3 subfractions. Furthermore, pre-β1-HDL particle levels were subnormal following removal (−53%) upon apheresis, suggesting that cellular cholesterol efflux may be defective in the immediate postapheresis period. In LDL-receptor (LDL-R) deficiency, LDL-apheresis may enhance flux through the reverse cholesterol transport pathway and equally attenuate potential biglycan-mediated deposition of apoE-HDL in the arterial matrix.http://www.sciencedirect.com/science/article/pii/S0022227520408351high density lipoprotein heterogeneityHDL proteomelow density lipoprotein receptor mutationspremature atherosclerosisapolipoprotein E |
| spellingShingle | Alexina Orsoni Samir Saheb Johannes H.M. Levels Geesje Dallinga-Thie Marielle Atassi Randa Bittar Paul Robillard Eric Bruckert Anatol Kontush Alain Carrié M. John Chapman LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection Journal of Lipid Research high density lipoprotein heterogeneity HDL proteome low density lipoprotein receptor mutations premature atherosclerosis apolipoprotein E |
| title | LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection |
| title_full | LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection |
| title_fullStr | LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection |
| title_full_unstemmed | LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection |
| title_short | LDL-apheresis depletes apoE-HDL and pre-β1-HDL in familial hypercholesterolemia: relevance to atheroprotection |
| title_sort | ldl apheresis depletes apoe hdl and pre β1 hdl in familial hypercholesterolemia relevance to atheroprotection |
| topic | high density lipoprotein heterogeneity HDL proteome low density lipoprotein receptor mutations premature atherosclerosis apolipoprotein E |
| url | http://www.sciencedirect.com/science/article/pii/S0022227520408351 |
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