Abstract
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.
Highlights
Phospholipid transfer protein (PLTP) is one of the major modulators of lipoprotein metabolism and atherosclerosis development in humans; we still do not quite understand the mechanisms
PLTP and cholesteryl ester transfer protein (CETP) show moderate homology of sequence [2] and similar structural features [1, 27], they show no overlap in their in vivo functions. This was demonstrated in our study by preparing CETP transgenic/PLTP KO mice; the expression of CETP had an additive effect on HDL lowering, resulting in markedly reduced HDL levels in the CETP transgenic/PLTP KO mice [28]
From liver-specific PLTP expressed mice, the major function of liver PLTP is to drive VLDL production and we proposed a model for PLTP activity-mediated apoB-containing triglyceride-rich lipoprotein (BLp) lipidation (Fig. 1) [13]
Summary
Phospholipid transfer protein (PLTP) belongs to the lipid transfer protein family, including cholesteryl ester transfer protein (CETP), lipopolysaccharide-binding protein, and bactericidal/permeability increasing protein (BPI) [1]. We prepared adipose tissue-specific PLTP KO mice and found that the mice showed significant decreases in plasma PLTP activity (20%) and cholesterol (18%), phospholipid (17%), and apoA-I (26%) levels [17]. 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
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