Remodeling of HDL remnants generated by scavenger receptor class B type I
Scavenger receptor class B type I (SR-BI) mediates the selective transfer of cholesteryl ester from HDL to cells. We previously established that SR-BI overexpressed in livers of apolipoprotein A-I-deficient mice processes exogenous human HDL2 to incrementally smaller HDL particles. When mixed with n...
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| Format: | Article |
| Language: | English |
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Elsevier
2004-09-01
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| Series: | Journal of Lipid Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S0022227520312839 |
| _version_ | 1819072310488858624 |
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| author | Nancy R. Webb Maria C. de Beer Bela F. Asztalos Nathan Whitaker Deneys R. van der Westhuyzen Frederick C. de Beer |
| author_facet | Nancy R. Webb Maria C. de Beer Bela F. Asztalos Nathan Whitaker Deneys R. van der Westhuyzen Frederick C. de Beer |
| author_sort | Nancy R. Webb |
| collection | DOAJ |
| description | Scavenger receptor class B type I (SR-BI) mediates the selective transfer of cholesteryl ester from HDL to cells. We previously established that SR-BI overexpressed in livers of apolipoprotein A-I-deficient mice processes exogenous human HDL2 to incrementally smaller HDL particles. When mixed with normal mouse plasma either in vivo or ex vivo, SR-BI-generated HDL “remnants” rapidly remodel to form HDL-sized lipoproteins. In this study, we analyzed HDLs throughout the process of HDL remnant formation and investigated the mechanism of conversion to larger particles. Upon interacting with SR-BI, α-migrating HDL2 is initially converted to a preα-migrating particle that is ultimately processed to a smaller α-migrating HDL remnant. SR-BI does not appear to generate preβ-1 HDL particles. When incubated with isolated lipoprotein fractions, HDL remnants are converted to lipoprotein particles corresponding in size to the particle incubated with the HDL remnant. HDL remnant conversion is not altered in phospholipid transfer protein (PLTP)-deficient mouse plasma or by the addition of purified PLTP. Although LCAT-deficient plasma promoted only partial conversion, this deficiency was attributable to the nature of HDL particles in LCAT−/− mice rather than to a requirement for LCAT in the remodeling process.We conclude that HDL remnants, generated by SR-BI, are converted to larger particles by rapidly reassociating with existing HDL particles in an enzyme-independent manner. |
| first_indexed | 2024-12-21T17:35:42Z |
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| id | doaj.art-0028b9e6010844e48992544c1f3091fd |
| institution | Directory Open Access Journal |
| issn | 0022-2275 |
| language | English |
| last_indexed | 2024-12-21T17:35:42Z |
| publishDate | 2004-09-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Lipid Research |
| spelling | doaj.art-0028b9e6010844e48992544c1f3091fd2022-12-21T18:55:45ZengElsevierJournal of Lipid Research0022-22752004-09-0145916661673Remodeling of HDL remnants generated by scavenger receptor class B type INancy R. Webb0Maria C. de Beer1Bela F. Asztalos2Nathan Whitaker3Deneys R. van der Westhuyzen4Frederick C. de Beer5Department of Internal Medicine, University of Kentucky Medical Center, Lexington, KY; Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA; Department of Veterans Affairs Medical Center, Lexington, KYDepartment of Internal Medicine, University of Kentucky Medical Center, Lexington, KY; Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA; Department of Veterans Affairs Medical Center, Lexington, KYDepartment of Internal Medicine, University of Kentucky Medical Center, Lexington, KY; Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA; Department of Veterans Affairs Medical Center, Lexington, KYDepartment of Internal Medicine, University of Kentucky Medical Center, Lexington, KY; Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA; Department of Veterans Affairs Medical Center, Lexington, KYDepartment of Internal Medicine, University of Kentucky Medical Center, Lexington, KY; Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA; Department of Veterans Affairs Medical Center, Lexington, KYDepartment of Internal Medicine, University of Kentucky Medical Center, Lexington, KY; Lipid Metabolism Laboratory, Jean Mayer United States Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston, MA; Department of Veterans Affairs Medical Center, Lexington, KYScavenger receptor class B type I (SR-BI) mediates the selective transfer of cholesteryl ester from HDL to cells. We previously established that SR-BI overexpressed in livers of apolipoprotein A-I-deficient mice processes exogenous human HDL2 to incrementally smaller HDL particles. When mixed with normal mouse plasma either in vivo or ex vivo, SR-BI-generated HDL “remnants” rapidly remodel to form HDL-sized lipoproteins. In this study, we analyzed HDLs throughout the process of HDL remnant formation and investigated the mechanism of conversion to larger particles. Upon interacting with SR-BI, α-migrating HDL2 is initially converted to a preα-migrating particle that is ultimately processed to a smaller α-migrating HDL remnant. SR-BI does not appear to generate preβ-1 HDL particles. When incubated with isolated lipoprotein fractions, HDL remnants are converted to lipoprotein particles corresponding in size to the particle incubated with the HDL remnant. HDL remnant conversion is not altered in phospholipid transfer protein (PLTP)-deficient mouse plasma or by the addition of purified PLTP. Although LCAT-deficient plasma promoted only partial conversion, this deficiency was attributable to the nature of HDL particles in LCAT−/− mice rather than to a requirement for LCAT in the remodeling process.We conclude that HDL remnants, generated by SR-BI, are converted to larger particles by rapidly reassociating with existing HDL particles in an enzyme-independent manner.http://www.sciencedirect.com/science/article/pii/S0022227520312839high density lipoproteincholesteryl esterselective lipid uptake |
| spellingShingle | Nancy R. Webb Maria C. de Beer Bela F. Asztalos Nathan Whitaker Deneys R. van der Westhuyzen Frederick C. de Beer Remodeling of HDL remnants generated by scavenger receptor class B type I Journal of Lipid Research high density lipoprotein cholesteryl ester selective lipid uptake |
| title | Remodeling of HDL remnants generated by scavenger receptor class B type I |
| title_full | Remodeling of HDL remnants generated by scavenger receptor class B type I |
| title_fullStr | Remodeling of HDL remnants generated by scavenger receptor class B type I |
| title_full_unstemmed | Remodeling of HDL remnants generated by scavenger receptor class B type I |
| title_short | Remodeling of HDL remnants generated by scavenger receptor class B type I |
| title_sort | remodeling of hdl remnants generated by scavenger receptor class b type i |
| topic | high density lipoprotein cholesteryl ester selective lipid uptake |
| url | http://www.sciencedirect.com/science/article/pii/S0022227520312839 |
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