Triglyceride increase in the core of high-density lipoproteins augments apolipoprotein dissociation from the surface: Potential implications for treatment of apolipoprotein deposition diseases

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• 作者：Shobini Jayaraman^a ; Jose Luis S&aacute ; nchez-Quesada^b ; Olga Gursky^a ; ^{gursky@bu.edu}
• 关键词：Apo ; apolipoprotein ; AApoAI ; apoA-I amyloidosis ; AApoAII ; apoA-II amyloidosis ; AA ; amyloid A ; SAA ; serum amyloid A ; HDL ; high-density lipoprotein ; VLDL ; very-low density lipoprotein ; rHDL ; reconstituted HDL ; TG ; triglyceride ; TO ; triolein ; CE ; cholesterol ester ; CETP ; cholesterol ester transfer protein ; UC ; unesterified cholesterol ; nHDL ; native single-donor HDL from plasma of healthy volunteers ; TG-HDL ; nHDL enriched with TG ; TO-HDL ; nHDL enriched with TO ; NL ; normolipidemic ; DM ; diabetes melli
• 刊名：Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：1863
• 期：1
• 页码：200-210
• 全文大小：1546 K
• 卷排序：1863

文摘

Apolipoproteins such as apoA-I, apoA-II and SAA can cause systemic amyloidoses. Binding to high-density lipoproteins protects these proteins from misfolding. Free apolipoproteins are intrinsically disordered and labile to misfolding. Increasing triglyceride levels in human or model HDL promotes protein release. Triglyceride-lowering therapies may potentially alleviate apolipoprotein amyloidoses.