Analysis of lipid transfer activity between model nascent HDL particles and plasma lipoproteins: implications for current concepts of nascent HDL maturation and genesis

The specifics of nascent HDL remodeling within the plasma compartment remain poorly understood. We developed an in vitro assay to monitor the lipid transfer between model nascent HDL (LpA-I) and plasma lipoproteins. Incubation of α-125I-LpA-I with plasma resulted in association of LpA-I with existing plasma HDL, whereas incubation with TD plasma or LDL resulted in conversion of α-125I-LpA-I to preβ-HDL. To further investigate the dynamics of lipid transfer, nascent LpA-I were labeled with cell-derived [3 H]cholesterol (UC) or [3H]phosphatidylcholine (PC) and incubated with plasma at 37°C. The majority of UC and PC were rapidly transferred to apolipoprotein B (apoB). Subsequently, UC was redistributed to HDL for esterification before being returned to apoB. The presence of a phospholipid transfer protein (PLTP) stimulator or purified PLTP promoted PC transfer to apoB. Conversely, PC transfer was abolished in plasma from PLTP−/− mice. Injection of 125I-LpA-I into rabbits resulted in a rapid size redistribution of 125I-LpA-I. The majority of [3H]UC from labeled r(HDL) was esterified in vivo within HDL, whereas a minority was found in LDL. These data suggest that apoB plays a major role in nascent HDL remodeling by accepting their lipids and donating UC to the LCAT reaction. The finding that nascent particles were depleted of their lipids and remodeled in the presence of plasma lipoproteins raises questions about their stability and subsequent interaction with LCAT. The specifics of nascent HDL remodeling within the plasma compartment remain poorly understood. We developed an in vitro assay to monitor the lipid transfer between model nascent HDL (LpA-I) and plasma lipoproteins. Incubation of α-125I-LpA-I with plasma resulted in association of LpA-I with existing plasma HDL, whereas incubation with TD plasma or LDL resulted in conversion of α-125I-LpA-I to preβ-HDL. To further investigate the dynamics of lipid transfer, nascent LpA-I were labeled with cell-derived [3 H]cholesterol (UC) or [3H]phosphatidylcholine (PC) and incubated with plasma at 37°C. The majority of UC and PC were rapidly transferred to apolipoprotein B (apoB). Subsequently, UC was redistributed to HDL for esterification before being returned to apoB. The presence of a phospholipid transfer protein (PLTP) stimulator or purified PLTP promoted PC transfer to apoB. Conversely, PC transfer was abolished in plasma from PLTP−/− mice. Injection of 125I-LpA-I into rabbits resulted in a rapid size redistribution of 125I-LpA-I. The majority of [3H]UC from labeled r(HDL) was esterified in vivo within HDL, whereas a minority was found in LDL. These data suggest that apoB plays a major role in nascent HDL remodeling by accepting their lipids and donating UC to the LCAT reaction. The finding that nascent particles were depleted of their lipids and remodeled in the presence of plasma lipoproteins raises questions about their stability and subsequent interaction with LCAT. The process of lipidation of apolipoprotein A-I (apoA-I) by the ABCA1 transporter is functionally important in the biogenesis of HDL and in regulating lipid transport and metabolism, which, in turn, is critical for normal human physiology. This process is believed to be one of the major mechanisms by which HDL may protect against atherosclerotic cardiovascular disease (1Brewer H.B. Santamarina-Fojo S. New insights into the role of the adenosine triphosphate-binding cassette transporters in high-density lipoprotein metabolism and reverse cholesterol transport.Am. J. Cardiol. 2003; 91: 3E-11EAbstract Full Text Full Text PDF PubMed Scopus (83) Google Scholar, 2Tall A.R. Plasma cholesteryl ester transfer protein.J. Lipid Res. 1993; 34: 1255-1274Abstract Full Text PDF PubMed Google Scholar). As a result, the molecular mechanisms underlying the origin of plasma HDL have been a subject of intense study. Although it is well established that the liver and intestine are major sources of newly secreted HDL (3Brunham L.R. Kruit J.K. Iqbal J. Fievet C. Timmins J.M. Page T.D. Coburn B.A. Bissada N. Staels B. Groen A.K. et al.Intestinal ABCA1 directly contributes to HDL biogenesis in vivo.J. Clin. Invest. 2006; 116: 1052-1062Crossref PubMed Scopus (425) Google Scholar, 4Timmins J.M. Lee J.Y. Boudyguina E. Kluckman K.D. Brunham L.R. Mulya A. Gebre A.K. Cutinho J.M. Colvin P.L. Smith T.L. et al.Targeted inactivation of hepatic Abca1 causes profound hypoalphalipoproteinemia and kidney hypercatabolism of apoA-I.J. Clin. Invest. 2005; 115: 1333-1342Crossref PubMed Scopus (427) Google Scholar), there is little information on the metabolism of nascent HDL, their interaction with resident plasma lipoproteins, and their effect on lipid transport. Although discoidal nascent HDLs are believed to be critical intermediates between lipid-poor apoA-I and mature spherical HDL, the accurate detection and analysis of these nascent particles has proven difficult because they are rapidly remodeled by plasma factors and are subsequently found at relatively low concentrations in the plasma of most species. Generally it is thought that upon entering the plasma, nascent HDL acquire phospholipids (PLs) and unesterified cholesterol (UCs) and associate with LCAT and other plasma factors, including phospholipid transfer protein (PLTP) and cholesteryl ester transfer protein (CETP), for the completion of the maturation cycle. The pioneering biophysical and biochemical studies by Forte and colleagues (5McCall M.R. Nichols A.V. Blanche P.J. Shore V.G. Forte T.M. Lecithin:cholesterol acyltransferase-induce transformation of HepG2 lipoproteins.J. Lipid Res. 1989; 30: 1579-1589Abstract Full Text PDF PubMed Google Scholar, 6Nichols A.V. Blanche P.J. Gong E.L. Shore V.G. Forte T.M. Molecular pathways in the transformation of model discoidal lipoprotein complexes induced by lecithin:cholesterol acyltransferase.Biochim. Biophys. Acta. 1985; 834: 285-300Crossref PubMed Scopus (54) Google Scholar, 7Thrift R.N. Forte T.M. Cahoon B.E. Shore V.G. Characterization of lipoproteins produced by the human liver cell line, HepG2, under defined conditions.J. Lipid Res. 1986; 27: 236-250Abstract Full Text PDF PubMed Google Scholar), have shown that nascent HDLs are defined by their ability to be transformed into mature plasma HDL by the action of LCAT. Indeed, LCAT alone appears sufficient to introduce heterogeneity into the size distribution of HDL particles. Newly secreted HDL generated by hepatocyte HepG2 are remarkably similar to HDL from with LCAT (5McCall M.R. Nichols A.V. Blanche P.J. Shore V.G. Forte T.M. Lecithin:cholesterol acyltransferase-induce transformation of HepG2 lipoproteins.J. Lipid Res. 1989; 30: 1579-1589Abstract Full Text PDF PubMed Google Scholar). of LCAT alone to these particles a studies from and B. J. Molecular and of apolipoprotein A-I lipidation by the cassette transporter Full Text Full Text PDF PubMed Scopus Google Scholar, S. Characterization of nascent HDL particles and by of lipids to Lipid Res. 2006; Full Text Full Text PDF PubMed Scopus Google Scholar, Lee A. J. analysis of and of apolipoprotein for of nascent lipoprotein Full Text Full Text PDF PubMed Scopus Google Scholar, S. S. J. and of nascent particles in cell Lipid Res. 2005; Full Text Full Text PDF PubMed Scopus Google have that incubation of apoA-I with cell ABCA1 to the of nascent particles in the HDL size The of these of nascent HDL has the in the pathways the and remodeling of nascent a Mulya et A. Lee J.Y. Gebre A.K. Boudyguina E. Smith T.L. Colvin P.L. interaction of apoA-I with ABCA1 in vivo of nascent Lipid Res. Full Text Full Text PDF PubMed Scopus Google a similar model of nascent HDL and that interaction of apoA-I with ABCA1 the in vivo of these particles. apolipoprotein lipid transfer between nascent HDL and other plasma lipoproteins the of the nascent particles and their subsequent remodeling within the plasma by and and colleagues A. unesterified cholesterol between HDLs and LDL for esterification in 1993; PubMed Scopus Google Scholar, A. S. cholesterol transport in plasma of with of HDL PubMed Scopus Google have shown that cell-derived UC between HDL and LDL for esterification in This is in with studies by and A. C. and of lecithin:cholesterol and cholesteryl ester transfer protein in plasma lipoproteins. for a these with A-I and that the esterification and transfer of cell-derived 1989; Full Text PDF PubMed Google that an of cholesterol and it into a of particles and to particles that LCAT for the between the cholesterol and nascent HDL remodeling has been studies to the and the specifics of the lipid transfer between model nascent HDL and plasma lipoproteins. the process of lipid transfer the remodeling of these nascent particles within the plasma were from with an was from the into were on before Plasma from disease were by of Plasma from with with were by from of Plasma from were from the for and of human are shown in plasma apoA-I was in and against apoA-I was with by to a of apoA-I and within (LpA-I) particles were S. S. J. and of nascent particles in cell Lipid Res. 2005; Full Text Full Text PDF PubMed Scopus Google Scholar). human were with and incubated with for at 37°C. were labeled with cholesterol or for with and incubated with apoA-I for at 37°C. or phospholipid LpA-I were and with a size was with LpA-I particles were further to The of LpA-I particles was by and within and cholesterol at a were the by and A. A. The of of and the size and of their lipoprotein 1993; Full Text PDF PubMed Google Scholar). UC was to a of HDL particles were by and against to apoA-I or lipid was by were within LpA-I particles generated by HepG2 were S. S. J. and of nascent particles in cell Lipid Res. 2005; Full Text Full Text PDF PubMed Scopus Google Scholar). HepG2 in were incubated with for 125I-LpA-I were and To 125I-LpA-I were further against a and at the of the was to The 125I-LpA-I was transferred to an and with an of of the The was to at for in a at The particles was by and was against HepG2 were labeled with of for and incubated with of apoA-I for particles were by The of LpA-I particles was by analysis with and within or LpA-I were incubated with plasma of plasma at for the in the presence or of LCAT PLTP stimulator or of LCAT and was by Gebre A.K. Characterization of human cholesterol Lipid Res. Full Text Full Text PDF PubMed Google Scholar, J. vitro factors the of in human Lipid Res. Full Text Full Text PDF PubMed Google Scholar). of PLTP by PLTP assay C. of human plasma phospholipid transfer protein and 2005; PubMed Scopus Google Scholar). LDL or was incubated with 125I-LpA-I for at 37°C. apoA-I was by LpA-I or LpA-I were incubated with plasma plasma at or for the in the or presence of or purified plasma apoB was with an of and the lipids from the and were ester [3H]phosphatidylcholine and were by and were for vivo studies were on New rabbits were an model because of of with and the presence of the plasma remodeling factors and were with or in the of the were from the of the and were on and at for at and concentrations were on an Molecular was by cholesterol in the of lipoproteins with from the by Plasma and apoB concentrations were by or by in nascent LpA-I was by concentrations in nascent LpA-I were by have A. A. J. of in disease B Lipid Res. 2005; Full Text Full Text PDF PubMed Scopus Google Scholar). and were J. vitro factors the of in human Lipid Res. Full Text Full Text PDF PubMed Google Scholar). and UC and cholesterol were to the plasma lipoproteins were by on a and cholesterol was LCAT was Gebre A.K. Characterization of human cholesterol Lipid Res. Full Text Full Text PDF PubMed Google Scholar). and PLTP were J. vitro factors the of in human Lipid Res. Full Text Full Text PDF PubMed Google Scholar, C. of human plasma phospholipid transfer protein and 2005; PubMed Scopus Google Scholar). plasma PLTP was purified J. J. C. transfer protein (PLTP) causes of apolipoprotein Lipid Res. Full Text Full Text PDF PubMed Google Scholar). were with were was for between LpA-I were generated by incubation of apoA-I with human in and As shown in of nascent LpA-I particles were These nascent particles with of These nascent LpA-I were and B. J. Molecular and of apolipoprotein A-I lipidation by the cassette transporter Full Text Full Text PDF PubMed Scopus Google Scholar, S. S. J. and of nascent particles in cell Lipid Res. 2005; Full Text Full Text PDF PubMed Scopus Google Scholar). The of nascent LpA-I was with which an size of analysis of LpA-I generated by human an UC to of the of phospholipid of LpA-I was and have B. J. Molecular and of apolipoprotein A-I lipidation by the cassette transporter Full Text Full Text PDF PubMed Scopus Google Scholar). The of LpA-I be to the of B. J. Molecular and of apolipoprotein A-I lipidation by the cassette transporter Full Text Full Text PDF PubMed Scopus Google Scholar, S. Characterization of nascent HDL particles and by of lipids to Lipid Res. 2006; Full Text Full Text PDF PubMed Scopus Google Scholar). of the apoA-I in LpA-I or of apoA-I have Lee A. J. analysis of and of apolipoprotein for of nascent lipoprotein Full Text Full Text PDF PubMed Scopus Google Scholar, J. New insights into the biogenesis of human high-density 2006; PubMed Scopus Google Scholar). We that the model of nascent HDL may be for the of apolipoprotein lipid transfer it to an in vivo nascent HDL of protein and lipid these model nascent particles to their cholesterol esterification S. S. J. and of nascent particles in cell Lipid Res. 2005; Full Text Full Text PDF PubMed Scopus Google Scholar), and similar particles were to investigate their in vivo in human apoA-I A. Lee J.Y. Gebre A.K. Boudyguina E. Smith T.L. Colvin P.L. interaction of apoA-I with ABCA1 in vivo of nascent Lipid Res. Full Text Full Text PDF PubMed Scopus Google Scholar). To the size distribution of model nascent LpA-I was by the presence of plasma lipoproteins, 125I-LpA-I were incubated with plasma plasma at for on the that the in vivo nascent HDL of plasma apoA-I J. J. HDL by hypercatabolism of mature apoA-I PubMed Scopus Google Scholar). As shown in incubated with plasma α-125I-LpA-I from of to rapidly associate with existing plasma lipoproteins This is with the size distribution of plasma particles with an in the of plasma HDL, the of TD LpA-I were to and particles in the presence of the majority of LpA-I were to whereas upon incubation with LpA-I were to particles in size to nascent 125I-LpA-I and similar of association with plasma We in the size distribution of LpA-I incubated alone for at with LpA-I at of and in and in a of the plasma factors and PLTP the of α-125I-LpA-I size distribution incubation with were in in the presence of a LCAT a or a PLTP stimulator As shown in in the presence of or the size distribution of 125I-LpA-I with plasma HDL This is with the that nascent 125I-LpA-I have similar association with normal and plasma plasma was by HDL particles by apoA-I incubation of 125I-LpA-I with a plasma in the presence of a PLTP stimulator resulted in the transformation of a of the 125I-LpA-I with particles to This was with the of plasma by apoA-I with plasma The presence of and resulted in the of LCAT and by and whereas PLTP by on the that nascent LpA-I were remodeled to including upon incubation with TD plasma or LDL the was the in the size distribution of LpA-I was by cholesterol transfer between nascent particles and plasma lipoproteins. To to developed an in vitro assay to monitor the dynamics of cholesterol transfer between nascent LpA-I and plasma lipoproteins, well were labeled with [3H]UC and incubated with apoA-I to nascent in and LpA-I were incubated with plasma plasma at for Subsequently, plasma apoB was with and the lipids from the and were [3H]UC and were by and for To that under the lipid transfer assay nascent LpA-I associate with plasma the assay was 125I-LpA-I. 125I-LpA-I was found with apoB a incubation Conversely, a analysis of cholesterol transfer that a the majority of [3H]UC from LpA-I was transferred to plasma which an incubation This was with a of [3H]UC from LpA-I at the the a of [3H]UC was esterified by LCAT within the HDL and was subsequently transferred to apoB by in a To the of [3H]UC between nascent and HDL the of UC and between plasma lipoproteins, the in UC and in the apoB and HDL was As shown in UC in plasma apoB was and incubation at whereas the of was and with the there was a in the of in HDL and incubation with Incubation at in the presence of the transfer of [3H]UC from LpA-I to apoB esterification of cholesterol that generated by incubation of with HepG2 were transformed to particles by with existing plasma HDL conversion to be of LCAT because the presence of with the LpA-I cell-derived [3H]UC from labeled were transferred to lipoproteins and subsequently esterified within plasma HDL Although the lipid of apoB within the plasma have been that LDL and at an phospholipid are of [3H]UC of by the transfer of to LDL in the of mature This is with the finding that the transfer of UC from LpA-I to plasma apoB was in the of mature HDL, the with TD are to the of apoB for the lipid We that incubation of 125I-LpA-I with plasma in the presence of a PLTP stimulator resulted in the conversion of a of 125I-LpA-I with to To the in LpA-I size distribution was by phospholipid of these the dynamics of phospholipid transfer between nascent LpA-I and plasma lipoproteins. LpA-I were labeled with cell-derived in and LpA-I were incubated with plasma plasma at for Plasma apoB was and and were by and for As shown in of of LpA-I was transferred to plasma apoB within a incubation at with a of transfer to apoB. the of from LpA-I was transferred to apoB a incubation To the PC of LpA-I was by PLTP were in the presence of a PLTP stimulator or purified human plasma As shown in and and purified PLTP the transfer of to apoB. Conversely, the transfer of from nascent LpA-I to LDL was in the presence of plasma from PLTP incubation of 125I-LpA-I with plasma from PLTP in the presence of resulted in the conversion of a of 125I-LpA-I with particles to transfer of nascent LpA-I PC and conversion to in the presence of plasma from LpA-I labeled with cell-derived was incubated with of human LDL in the presence of plasma from normal or for at in the presence or of PLTP stimulator apoB was with lipid with apoB was by and for are of 125I-LpA-I was incubated with plasma from normal or in the presence of for at 37°C. apoA-I was by were by and was directly by 125I-LpA-I incubated in for at is shown Molecular size are an to the to which the of LpA-I size distribution in nascent 125I-LpA-I or were into and the in the size distribution were by This was to in the in vivo of nascent to to the in vitro data 125I-LpA-I and were in and and rabbits were with or 125I-LpA-I which of the plasma apoA-I in rabbits P.J. of apoA-I protein or of discoidal and spherical studies in and hepatic PubMed Scopus Google Scholar). was from rabbits at the and the size was by As shown in at the the nascent 125I-LpA-I with of rapidly with and of particles a of apoA-I was from to particles with This is with the size distribution of particles with an the nascent 125I-LpA-I with were to particles the was rapidly into existing and distribution was the of the To further the transfer of unesterified cholesterol from nascent HDL particles to lipoproteins in in which have lipoprotein with mice. [3H]UC r(HDL) because of the to sufficient [3H]UC of were with of which of the plasma apoA-I in rabbits P.J. of apoA-I protein or of discoidal and spherical studies in and hepatic PubMed Scopus Google Scholar). analysis that r(HDL) with a of was at the and to As shown in at the the majority of was found within the with a found in the LDL the was in the HDL size The distribution of by lipoproteins was to the distribution of lipoprotein cholesterol in the in the HDL in LDL and HDL the of analysis of [3H]UC and in plasma at the of cholesterol was esterified As on lipoprotein the majority of was found with the HDL the a of [3H]UC was found with which LDL in in a and esterification of HDL into were at the of r(HDL) in and lipid [3H]UC and were by and for The of of at the was are of were to a and the of [3H]UC and in the HDL and LDL was by of was found in the HDL is thought that entering plasma, nascent HDL acquire unesterified cholesterol and associate with to their conversion to mature the and of that in vitro incubation of model nascent LpA-I with human plasma the LpA-I size distribution by rapid association of LpA-I with existing plasma in the of HDL or in the presence of the majority of nascent LpA-I were remodeled to particles and This is with by and A. of high-density lipoprotein a of or LDL Biophys. Acta. PubMed Scopus Google Scholar), r(HDL) major upon of LDL. is that the interaction of nascent LpA-I with plasma lipoproteins may to of apoA-I from the nascent particles they are depleted of lipid to lipid-poor apoA-I including and Subsequently, these particles associate rapidly with the resident plasma HDL This is by the in vitro lipid transfer assay that the majority of UC of nascent LpA-I was rapidly transferred to plasma lipoproteins and subsequently redistributed to HDL for esterification by LCAT before being transferred to apoB by the the PC of nascent LpA-I was transferred to plasma lipoproteins the finding that the of [3H]UC between nascent and HDL the of UC and between plasma lipoproteins the that UC is transferred from nascent LpA-I to plasma lipoproteins of with Although the lipid transfer of these model nascent particles within the plasma have been have the lipid transfer under in This is on the that the nascent HDL the of apoA-I in which of plasma apoA-I J. J. HDL by hypercatabolism of mature apoA-I PubMed Scopus Google Scholar). finding that most of the nascent LpA-I [3H]UC is transferred to apoB within of incubation is in with a that the majority of cell-derived [3H]UC is transferred to LDL of with UC A. unesterified cholesterol between HDLs and LDL for esterification in 1993; PubMed Scopus Google Scholar). normal plasma, of UC is in LDL. Although the between the transfer of [3H]UC and from LpA-I to plasma apoB is that [3H]UC transfer to apoB was at whereas transfer was This is with the finding that PLTP the transfer of from LpA-I to plasma apoB and the conversion of nascent LpA-I to and are in with studies by and colleagues A. transfer from low lipoproteins to lipoproteins is by the and concentrations of 34: PubMed Scopus Google Scholar, A. Lipid between lipoprotein complexes and low of plasma protein Lipid Res. Full Text PDF PubMed Google Scholar), that with PLTP the transfer of phospholipids from r(HDL) to LDL to discoidal particles. the transfer of cholesterol and phospholipid between r(HDL) and LDL has been found to be by the and concentrations of the and particles. similar by and of LpA-I and on cholesterol transfer between lipoproteins.J. Full Text Full Text PDF PubMed Scopus Google that the of cholesterol transfer from r(HDL) to LDL are in the in for the r(HDL) This that the lipid transfer process be by a by Nichols and of transfer to the of transfer between PubMed Scopus Google Scholar). is that the and of nascent well the interaction with plasma factors, including have a effect on lipid transfer to other plasma lipoproteins. This is in with studies that phospholipids and PLTP a role in HDL remodeling and J. S. A. C. plasma phospholipid transfer protein causes lipoprotein 1993; Full Text PDF PubMed Google Scholar, J. C. A. of phospholipid transfer protein and cholesteryl ester transfer protein to the of J. PubMed Scopus Google Scholar, N. C. J. The of the remodeling of lipoproteins by phospholipid transfer protein.J. Full Text Full Text PDF PubMed Scopus Google Scholar, A. J. C. S. C. transfer protein conversion of lipoproteins Biophys. Acta. PubMed Scopus Google Scholar). the molecular of nascent HDL remodeling in vivo is for HDL We that of nascent LpA-I into rabbits resulted in a rapid in the LpA-I size distribution with HDL This is in with a by Mulya et A. Lee J.Y. Gebre A.K. Boudyguina E. Smith T.L. Colvin P.L. interaction of apoA-I with ABCA1 in vivo of nascent Lipid Res. Full Text Full Text PDF PubMed Scopus Google that that a similar model of nascent LpA-I was rapidly remodeled in human apoA-I mice. nascent LpA-I particles were remodeled to LpA-I particles were turn, resulted in liver and kidney the apoB in rabbits with which a to of lipid transfer between nascent LpA-I and that the [3H]UC of r(HDL) was rapidly redistributed to and particles that [3H]UC with HDL was rapidly esterified and a of was transferred to LDL studies are in and which are by LDL to the lipid transfer process between nascent HDL and apoB. studies by and A. C. and of lecithin:cholesterol and cholesteryl ester transfer protein in plasma lipoproteins. for a these with A-I and that the esterification and transfer of cell-derived 1989; Full Text PDF PubMed Google have that a of human HDL that with on cholesterol from at a HDL, which the of plasma it was that particles were in the of Characterization of lipoproteins. for the of apoA-I with Lipid Res. Full Text PDF PubMed Google and the P.J. Molecular mechanisms of reverse cholesterol PubMed Scopus Google Scholar), a role for these particles in the of suggest that generated by HepG2 nascent particles in donating their UC to plasma apoB and with existing plasma HDL of LCAT is that other plasma factors be in the conversion of to particles. This is by finding that the conversion of nascent LpA-I to HDL was found to be in TD plasma Indeed, an by et A. S. C. of and conversion into for HDL conversion in PubMed Scopus Google that normal plasma a that to that is in TD Although the of nascent LpA-I to mature HDL are raises important questions the stability of nascent particles in the plasma the nascent particles with LCAT they are depleted of their cholesterol and phospholipid in the presence of other the newly HDL in the plasma compartment their apoA-I and lipid are into the resident plasma HDL and is the of nascent particles their association with the resident plasma HDL The that the UC and PC of LpA-I were transferred to lipoproteins and subsequently to HDL that LDL plays a role in nascent HDL This is in with studies that apoB of UC upon entering the plasma UC from cell of cholesteryl of low lipoproteins.J. Clin. Invest. PubMed Scopus Google Scholar, A. and of nascent lipoproteins from purified Lipid Res. Full Text PDF PubMed Google Scholar). is well that LCAT plays a role in the reverse cholesterol transport process by a cholesterol between cell and the plasma compartment A.R. Plasma lipoproteins. and to Clin. Invest. PubMed Scopus Google Scholar). The transfer of UC from nascent particles to which is the LDL may an reverse cholesterol transport This is by the that the in vitro transfer of UC from nascent LpA-I to apoB was in the presence of LCAT This is in with studies that LDL of with LCAT of that the in vivo transfer of UC to LDL in the of LCAT A. S. cholesterol transport in plasma of with of HDL PubMed Scopus Google Scholar). This has a biochemical of the nascent HDL remodeling that plasma lipoproteins and As in the UC of the model nascent HDL was transferred to plasma which was redistributed to HDL for esterification by LCAT. Subsequently, were transferred to apoB by the PLTP the of the PC of nascent HDL, to the of lipid-poor apoA-I into the plasma resident HDL or conversion to remodeling of the HDL resident by and PLTP contributes to the of or questions the stability and of the nascent particles within the plasma the of which further The and for plasma from disease plasma from and with apolipoprotein cholesteryl ester cholesteryl ester transfer protein nascent phospholipid phospholipid transfer protein disease unesterified cholesterol

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