Phospholipid Transfer Protein Is Expressed in Cerebrovascular Endothelial Cells and Involved in High Density Lipoprotein Biogenesis and Remodeling at the Blood-Brain Barrier

Manavalan, Anil Paul Chirackal; Kober, Alexandra; Metso, Jari; Lang, Ingrid; Becker, Tatjana; Hasslitzer, Karin; Zandl, Martina; Fanaee-Danesh, Elham; Pippal, Jyotsna B.; Sachdev, Vinay; Kratky, Dagmar; Štefulj, Jasminka; Jauhiainen, Matti; Panzenboeck, Ute

doi:10.1074/jbc.m113.499129

Cited by 31 publications

(23 citation statements)

References 61 publications

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“…PLTP deletion was demonstrated to increase amyloid--induced memory deficits in mice (24). Compared with the whole brain, the PLTP mRNA expression level is 6.8-fold higher in cerebral vessels (25) and PLTP may play a role in maintaining blood-brain barrier integrity, possibly through its ability to transfer vitamin E and modulate cerebrovascular oxidative stress (26). These findings collectively suggest a significant role of PLTP in both physiological and pathophysiological processes in the brain.…”

Section: Phospholipid Transfer Proteinmentioning

confidence: 98%

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Jiang

2018

Journal of Lipid Research

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Phospholipid transfer protein (PLTP) is one of the major modulators of lipoprotein metabolism and atherosclerosis development in humans; however, we still do not quite understand the mechanisms. In mouse models, PLTP overexpression induces atherosclerosis, while its deficiency reduces it. Thus, mouse models were used to explore the mechanisms. In this review, I summarize the major progress made in the PLTP research field and emphasize its impact on lipoprotein metabolism and atherosclerosis, as well as its regulation.

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Section: Phospholipid Transfer Proteinmentioning

confidence: 98%

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Jiang

2018

Journal of Lipid Research

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“…Lecithin-cholesterol acyltransferase (LCAT) esterifies the incorporated cholesterol, converting the ndHDL to HDL3 (Sorci-Thomas et al, 1990). The assembly of 2 small, dense, HDL3 molecules, in the presence of phospholipid transfer protein (PLTP), induces the formation of a larger HDL2 molecule (Chirackal Manavalan et al, 2014), which can be reversed by hepatic lipase (HL) (Patsch et al, 1987). Cholesterol esters can enter the liver directly via the receptor SR-B1, or via CETP, which facilitates the 1:1 exchange of cholesterol esters from HDL2 with TAGs from very low density lipoprotein (VLDL) and LDL .…”

Section: Overview Of Cholesterol Metabolismmentioning

confidence: 99%

Mathematically modelling the dynamics of cholesterol metabolism and ageing

et al. 2016

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“…On peripheral cells or in atherosclerotic plaque, PLTP promotes the binding of HDL to cholesterol-laden macrophages and fi broblasts and assists in HDL remodeling, which improves cholesterol and phospholipid removal ( 23 ). Recent evidence demonstrated that in vitro RNA interference silencing of PLTP decreased apoA1-and HDL3-mediated cholesterol effl ux by 67 and 30%, respectively, highlighting the potential role of PLTP in RCT ( 24 ).…”

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confidence: 99%

PLTP activity inversely correlates with CAAD: effects of PON1 enzyme activity and genetic variants on PLTP activity

Kim

Burt

Ranchalis

et al. 2015

Journal of Lipid Research

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Cholesterol carried on HDL (HDL-C) has long been believed to be cardioprotective, based on consistent epidemiologic fi ndings of an inverse relationship between incident CVD and HDL-C levels in subjects healthy at baseline ( 1, 2 ). Estimates from the Framingham Heart Study found that risk of myocardial infarction (MI) increased by 25% for each 5 mg/dl decrease in HDL-C below median values of HDL-C for both healthy men and women ( 2 ). Similar fi ndings of the cardioprotective effects of HDL-C have also been reported in subjects with CVD at baseline ( 3 ).In confl ict with these epidemiologic fi ndings, recent attempts to establish a causal relationship between HDL-C Abstract Recent studies have failed to demonstrate a causal cardioprotective effect of HDL cholesterol levels, shifting focus to the functional aspects of HDL. Phospholipid transfer protein (PLTP) is an HDL-associated protein involved in reverse cholesterol transport. This study sought to determine the genetic and nongenetic predictors of plasma PLTP activity (PLTPa), and separately, to determine whether PLTPa predicted carotid artery disease (CAAD). PLTPa was measured in 1,115 European ancestry participants from a casecontrol study of CAAD. A multivariate logistic regression model was used to elucidate the relationship between PLTPa and CAAD. Separately, a stepwise linear regression determined the nongenetic clinical and laboratory characteristics that best predicted PLTPa. A fi nal stepwise regression considering both nongenetic and genetic variables identifi ed the combination of covariates that explained maximal PLTPa variance. PLTPa was signifi cantly associated with CAAD (7.90 × 10 ؊ 9 ), with a 9% decrease in odds of CAAD per 1 unit increase in PLTPa (odds ratio = 0.91). Triglyceride levels ( P = 0.0042), diabetes ( P = 7.28 × 10 ؊ 5 ), paraoxonase 1 (PON1) activity ( P = 0.019), statin use ( P = 0.026), PLTP SNP rs4810479 ( P = 6.38 × 10 ؊ 7 ), and PCIF1 SNP rs181914932 ( P = 0.041) were all signifi cantly associated with PLTPa. PLTPa is signifi cantly inversely correlated with CAAD. Furthermore, we report a novel association between PLTPa and PON1 activity, a known predictor of

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Phospholipid Transfer Protein Is Expressed in Cerebrovascular Endothelial Cells and Involved in High Density Lipoprotein Biogenesis and Remodeling at the Blood-Brain Barrier

Cited by 31 publications

References 61 publications

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Phospholipid transfer protein: its impact on lipoprotein homeostasis and atherosclerosis

Mathematically modelling the dynamics of cholesterol metabolism and ageing

PLTP activity inversely correlates with CAAD: effects of PON1 enzyme activity and genetic variants on PLTP activity

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