Molecular and Macromolecular Specificity of Human Plasma Phospholipid Transfer Protein

Rao, Reena; Albers, John J.; Wolfbauer, Gertrud; Pownall, Henry J.

doi:10.1021/bi962776b

Cited by 105 publications

(88 citation statements)

References 40 publications

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“…When these results are considered with the data in Table IV, it follows that enrichment with TG destabilizes the apoA-I in rHDL. DISCUSSION The ability of PLTP to remodel HDL into large and small particles, mediate the dissociation of apoA-I from HDL, and transfer phospholipids between HDL and other lipoproteins is well documented (1)(2)(3)(4)(5)(6)(7)(8). Earlier work from this laboratory has also established that TG enrichment enhances the remodeling of HDL by PLTP (9).…”

Section: H (Closed Triangles)mentioning

confidence: 86%

“…1 transfers phospholipids (PL) between high density lipoproteins (HDL) and very low density lipoproteins as well as between different particles within the HDL fraction (1,2). It also remodels HDL into large and small particles in a process that is accompanied by the dissociation of lipid-poor or lipid-free apolipoprotein A-I (apoA-I) (3)(4)(5)(6)(7)(8).…”

Section: Phospholipid Transfer Protein (Pltp)mentioning

confidence: 99%

See 1 more Smart Citation

The Mechanism of the Remodeling of High Density Lipoproteins by Phospholipid Transfer Protein

Settasatian¹,

Duong²,

Curtiss³

et al. 2001

Journal of Biological Chemistry

115

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Phospholipid transfer protein (PLTP) remodels high density lipoproteins (HDL) into large and small particles. It also mediates the dissociation of lipid-poor or lipid-free apolipoprotein A-I (apoA-I) from HDL. Remodeling is enhanced markedly in triglyceride (TG)-enriched HDL (Rye, K.-A., Jauhiainen, M., Barter, P. J., and Ehnholm. C. (1998) J. Lipid. Res. 39, 613-622). This study defines the mechanism of the remodeling of HDL by PLTP and determines why it is enhanced in TG-enriched HDL. Homogeneous populations of spherical reconstituted HDL (rHDL) containing apoA-I and either cholesteryl esters only (CE-rHDL; diameter 9.3 nm) or CE and TG in their core (TG-rHDL; diameter 9.5 nm) were used. After 24 h of incubation with PLTP, all of the TG-rHDL, but only a proportion of the CE-rHDL, were converted into large (11.3-nm diameter) and small (7.7-nm diameter) particles. Only small particles were formed during the first 6 h of incubation of CE-rHDL with PLTP. The large particles and dissociated apoA-I were apparent after 12 h. In the case of TG-rHDL, small particles appeared after 1 h of incubation, while dissociated apoA-I and large particles were apparent at 3 h. The composition of the large particles indicated that they were derived from a fusion product. Spectroscopic studies indicated that the apoA-I in TG-rHDL was less stable than the apoA-I in CE-rHDL. In conclusion, these results show that (i) PLTP mediates rHDL fusion, (ii) the fusion product rearranges by two independent processes into small and large particles, and (iii) the more rapid remodeling of TG-rHDL by PLTP may be due to the destabilization of apoA-I. Phospholipid transfer protein (PLTP)1 transfers phospholipids (PL) between high density lipoproteins (HDL) and very low density lipoproteins as well as between different particles within the HDL fraction (1, 2). It also remodels HDL into large and small particles in a process that is accompanied by the dissociation of lipid-poor or lipid-free apolipoprotein A-I (apoA-I) (3-8). Remodeling is enhanced markedly in HDL that contain triglyceride (TG) in their core (9). Evidence of the importance of PLTP in HDL metabolism comes from studies of mice transgenic for human PLTP. These animals have increased levels of pre-␤ 1 -migrating HDL, the initial acceptors of cellular cholesterol in the first step of the reverse cholesterol pathway, and are also resistant to intracellular cholesterol accumulation (10 -12). Studies of PLTP knockout mice have shown that PLTP is essential for maintaining normal HDL levels in plasma (13). Moreover, it has been reported recently that PLTP-mediated transfers of phospholipids between HDL and other lipoprotein classes are not interchangeable with the phospholipid transfers that are mediated by cholesteryl ester transfer protein (CETP) (14).The mechanism of the remodeling of HDL by PLTP is poorly understood. Although there is evidence that particle fusion and the dissociation of lipid-poor or lipid-free apoA-I are involved (7,8), nothing is known about how the interaction of PLTP wi...

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Section: H (Closed Triangles)mentioning

confidence: 86%

Section: Phospholipid Transfer Protein (Pltp)mentioning

confidence: 99%

The Mechanism of the Remodeling of High Density Lipoproteins by Phospholipid Transfer Protein

Settasatian¹,

Duong²,

Curtiss³

et al. 2001

Journal of Biological Chemistry

115

View full text Add to dashboard Cite

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“…Phosphatidylcholines, a class of phospholipids, are the essential cholesterol-solubilizing components of HDL and the acyl donors for the esterification of FC into CE by LCAT (Rao et al, 1997). The elevated plasma PLTP activity during the negative energy balance in early lactation could represent a physiological reaction to counteract the low plasma cholesterol concentration by providing substrate for the LCAT reaction and thereby increasing the CE production in plasma.…”

Section: Discussionmentioning

confidence: 99%

Cholesterol metabolism, transport, and hepatic regulation in dairy cows during transition and early lactation

Kessler

Gross

Bruckmaier

et al. 2014

Journal of Dairy Science

121

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The transition from the nonlactating to the lactating state represents a critical period for dairy cow lipid metabolism because body reserves have to be mobilized to meet the increasing energy requirements for the initiation of milk production. The purpose of this study was to provide a comprehensive overview on cholesterol homeostasis in transition dairy cows by assessing in parallel plasma, milk, and hepatic tissue for key factors of cholesterol metabolism, transport, and regulation.

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“…Another early study found a larger proportion of SM in plasma chylomicrons than in chyle chylomicrons in humans, 12% versus 7% of the polar lipids (164), and in rat the proportion of SM is higher in plasma VLDL than in nascent VLDL (94,165). Whether this difference should be attributed to the action of lipases or differences in kinetics for the transfer of different polar lipids between lipoprotein classes is not known, although PLTP mediates the transfer of SM as well as glycerophospholipids (159,166). When VLDL was incubated with LPL, the level of g-migrating lipoprotein E increased, suggesting that these particles may be formed from surface material during lipolysis (167).…”

Section: Chylomicron and Vldl Smmentioning

confidence: 99%

Absorption and lipoprotein transport of sphingomyelin

Nilsson

Duan

2006

Journal of Lipid Research

227

201

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Dietary sphingomyelin (SM) is hydrolyzed by intestinal alkaline sphingomyelinase and neutral ceramidase to sphingosine, which is absorbed and converted to palmitic acid and acylated into chylomicron triglycerides (TGs). SM digestion is slow and is affected by luminal factors such as bile salt, cholesterol, and other lipids. In the gut, SM and its metabolites may influence TG hydrolysis, cholesterol absorption, lipoprotein formation, and mucosal growth. SM accounts for z20% of the phospholipids in human plasma lipoproteins, of which two-thirds are in LDL and VLDL. It is secreted in chylomicrons and VLDL and transferred into HDL via the ABCA1 transporter. Plasma SM increases after periods of large lipid loads, during suckling, and in type II hypercholesterolemia, cholesterol-fed animals, and apolipoprotein E-deficient mice. SM is thus an important amphiphilic component when plasma lipoprotein pools expand in response to large lipid loads or metabolic abnormalities. It inhibits lipoprotein lipase and LCAT as well as the interaction of lipoproteins with receptors and counteracts LDL oxidation. The turnover of plasma SM is greater than can be accounted for by the turnover of LDL and HDL particles. Some SM must be degraded via receptor-mediated catabolism of chylomicron and VLDL remnants and by scavenger receptor class B type I receptor-mediated transfer into cells. Sphingomyelin (SM) in mammalian cells is colocalized with cholesterol mainly in the plasma membrane and in lysosomal and Golgi membranes. It interacts strongly with cholesterol, and the regulation of SM and cholesterol metabolism are in part coordinated (1, 2). In plasma lipoproteins, SM is the second most abundant polar lipid after phosphatidylcholine (PC). The size of the plasma lipoprotein SM pool in humans is 1-1.5 g, of which approximately two-thirds are in apolipoprotein B (apoB)-containing triglyceride (TG)-rich lipoproteins and LDL. The SM content in most extraneural tissues is 1-2 g/kg. Factors regulating plasma SM concentration have received little attention. It was early shown that the level of SM is increased in hypercholesterolemia and that SM-rich lipoproteins accumulate in arteriosclerotic lesions (3-5). Plasma SM is thus a risk factor for ischemic heart disease (6), and the apoE-deficient (apoE 2/2 ) mouse, which accumulates SM-rich remnant particles in blood (7), has emerged as an important model for studying the role of SM in atherogenesis. The effects of lipoprotein SM in the arterial wall during atherogenesis may be related both to the modification of lipoproteins and to the generation of sphingolipid messengers (i.e., ceramide, ceramide-1-phosphate, sphingosine, and sphingosine-1-phosphate) initiated by SM hydrolysis (8-10). The role of SM metabolites in cell signaling has been the subject of several recent reviews (11)(12)(13)(14)(15)(16). Sphingolipid signals are triggered by numerous stimuli and mediate effects on cell growth and apoptosis and on the activities of inflammatory cells that may be pathogenic as well as protect...

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Molecular and Macromolecular Specificity of Human Plasma Phospholipid Transfer Protein

Cited by 105 publications

References 40 publications

The Mechanism of the Remodeling of High Density Lipoproteins by Phospholipid Transfer Protein

The Mechanism of the Remodeling of High Density Lipoproteins by Phospholipid Transfer Protein

Cholesterol metabolism, transport, and hepatic regulation in dairy cows during transition and early lactation

Absorption and lipoprotein transport of sphingomyelin

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