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PXD029713

PXD029713 is an original dataset announced via ProteomeXchange.

Dataset Summary
TitleApolipoprotein F in hyperlipidemia
DescriptionApolipoprotein F (ApoF) modulates lipoprotein metabolism by selectively inhibiting cholesteryl ester transfer protein (CETP) activity on LDL. This ApoF activity requires that it is bound to LDL. How hyperlipidemia alters total plasma ApoF and its binding to LDL are poorly understood. In this study, total ApoF and LDL-bound ApoF were quantified by ELISA. Plasma ApoF is increased 34% in hypercholesterolemic plasma. In hypertriglyceridemic plasma, ApoF was statistically unchanged. However, in donors with combined hypercholesterolemia and hypertriglyceridemia, the elevated triglyceride ameliorated the rise in ApoF caused by hypercholesterolemia alone. Compared to normolipidemic LDL, hypercholesterolemic LDL contained ~2-fold more ApoF per LDL particle, whereas ApoF bound to LDL in hypertriglyceridemia plasma was < 20% of control. To understand the basis for altered association of ApoF with hyperlipidemic LDL, the physiochemical properties of LDL were modified in vitro by CETP ± LCAT activities. The time-dependent change in LDL lipid composition, proteome, core and surface lipid packing, LDL surface charge, and LDL size caused by these factors were compared with the ApoF binding capacity of these LDL. Only LDL particle size correlated with ApoF binding capacity. This positive association between LDL size and ApoF content was confirmed in hyperlipidemic plasmas. Similarly, when in vitro-produced, enlarged LDL with elevated ApoF binding capacity were incubated with LPL to reduce their size, ApoF binding was reduced by 90%. Thus, plasma ApoF levels and the activation status of this ApoF are differentially altered by hypercholesterolemia and hypertriglyceridemia. LDL size is a key determinate of ApoF binding and activation.
HostingRepositoryPRIDE
AnnounceDate2022-02-11
AnnouncementXMLSubmission_2022-02-11_06:44:56.495.xml
DigitalObjectIdentifier
ReviewLevelPeer-reviewed dataset
DatasetOriginOriginal dataset
RepositorySupportUnsupported dataset by repository
PrimarySubmitterLing Li
SpeciesList scientific name: Homo sapiens (Human); NCBI TaxID: 9606;
ModificationListacetylated residue; monohydroxylated residue; iodoacetamide derivatized residue
InstrumentLTQ Orbitrap Elite
Dataset History
RevisionDatetimeStatusChangeLog Entry
02021-11-12 06:07:20ID requested
12022-02-11 06:44:56announced
Publication List
Dataset with its publication pending
Keyword List
submitter keyword: Apolipoproteins, plasma lipid transfer proteins, LDL metabolism, apolipoprotein F, cholesteryl ester transfer protein, lipid biochemistry, lipoproteins, hypercholesterolemia, hypertriglyceridemia
Contact List
Richard E. Morton
contact affiliationDepartment of Cardiovascular and Metabolic Sciences, NC10, Lerner Research Institute, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland, OH 44195
contact emailmortonr@ccf.org
lab head
Ling Li
contact affiliationCleveland Clinic
contact emaillil5@ccf.org
dataset submitter
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Dataset FTP location
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