Synthesis of recombinant high density lipoprotein with apolipoprotein A-I and apolipoprotein A-V
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Xinbo Zhang
Abstract
It has been shown that apolipoprotein A-V (apoA-V) over-expression significantly lowers plasma triglyceride levels and decreases atherosclerotic lesion development. To assess the feasibility of recombinant high density lipoprotein (rHDL) reconstituted with apoA-V and apolipoprotein A-I (apoA-I) as a therapeutic agent for hyperlipidemic disorder and atherosclerosis, a series of rHDL were synthesized in vitro with various mass ratios of recombinant apoA-I and apoA-V. It is interesting to find that apoA-V of rHDL had no effect on lipoprotein lipase (LPL) activation in vitro and very low density lipoprotein (VLDL) clearance in HepG2 cells and in vivo. By contrast, LPL activation and VLDL clearance were inhibited by the addition of apoA-V to rHDL. Furthermore, the apoA-V of rHDL could not redistribute from rHDL to VLDL after incubation at 37°C for 30 min. These findings suggest that an increase of apoA-V in rHDL could not play a role in VLDL clearance in vitro and in vivo, which could, at least in part, attribute to the lost redistribution of apoA-V from rHDL to VLDL and LPL binding ability of apoA-V in rHDL. The therapeutic application of rHDL reconstituted with apoA-V and apoA-I might need the construction of rHDL from which apoA-V could freely redistribute to VLDL.
©2011 by Walter de Gruyter Berlin New York
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Articles in the same Issue
- Review
- Recent insights into regulation of transcription by RNA polymerase III and the cellular functions of its transcripts
- Genes and Nucleic Acids
- Post-transcriptional regulation of human cathepsin L expression
- Protein Structure and Function
- In vitro conversion and seeded fibrillization of posttranslationally modified prion protein
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- Screening for small molecule modulators of Hsp70 chaperone activity using protein aggregation suppression assays: inhibition of the plasmodial chaperone PfHsp70-1
- Molecular Medicine
- Inhibition of AP-1 suppresses cervical cancer cell proliferation and is associated with p21 expression
- STAT3 controls matrix metalloproteinase-1 expression in colon carcinoma cells by both direct and AP-1-mediated interaction with the MMP-1 promoter
- Cell Biology and Signaling
- TGFβ1 suppresses vascular smooth muscle cell motility by expression of N-cadherin
- Renal pro-apoptotic proteins are reduced by growth hormone resistance but not by visceral fat removal
- Proteolysis
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