کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8311205 | 1538659 | 2015 | 41 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Paraoxonase 1 and HDL maturation
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کلمات کلیدی
SAAHigh-density lipoprotein subclassesHDL-CCETPDNTBPON1sdLDLHDLPLTPLCATApoA-ILDL-CVLDLnuclear magnetic resonance - رزونانس مغناطیسی هستهایMPO - DFOArylesterase - آریلسترازApolipoprotein A-I - آپولیپوپروتئین A-Icoronary heart disease - بیماری عروق کرونر قلبcardiovascular disease - بیماری قلب و عروقیTriglycerides - تریگلیسریدNMR - تشدید مغناطیسی هستهای Cardiovascular risk - خطر قلبی و عروقیCVD - رسوب دهی شیمیایی بخار serum amyloid A - سرم آمیلوئید ACAD - طراحی به کمک رایانه یا کَدUltracentrifugation - فوق ستاره سازیLactonase - لاکتونازlecithin: cholesterol acyltransferase - لسیتین: آستیلترانسفراز کلسترولhigh density lipoprotein - لیپوپروتئین با چگالی بالاvery low density lipoprotein - لیپوپروتئین چگالی بسیار کم استlow density lipoprotein - لیپوپروتئین چگالی کمLDL - لیپوپروتئین کم چگالی(کلسترول بد)myeloperoxidase - میلوپراکسیداز Paraoxonase 1 - پاراکسوناز 1cholesteryl ester transfer protein - پروتئین انتقال پروتئین کلسترول استhigh density lipoprotein cholesterol - کلسترول لیپوپروتئین با چگالی بالاlow density lipoprotein cholesterol - کلسترول لیپوپروتئین با چگالی کم
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Understanding the kinetics and function of paraoxonase 1 (PON1) is becoming an important issue in atherosclerosis. Low PON1 activity has been consistently linked with an increased risk of major cardiovascular events in the setting of secondary prevention of coronary artery disease. Recent studies have shown that there is a specific interaction of myeloperoxidase (MPO)-apoAI-PON1 on HDL surface that seems to be germane to atherogenesis. MPO specifically inhibits PON1 and PON1 mitigates MPO effects. Surprisingly, very little is known about the routes by which PON1 gets integrated into HDL or its fate during HDL remodeling in the intravascular space. We have developed a method that assesses PON1 activity in the individual HDL subclasses with the aid of which we have shown that PON1 is present across the HDL particle range and preferentially in HDL3, confirming data from ultracentrifugation (UC) studies. Upon HDL maturation ex vivo PON1 is activated and it shows a flux to both smaller and larger HDL particles as well as to VLDL and sdLDL. At the same time apoE, AI and AII are shifted across particle sizes. PON1 activation and flux across HDL particles are blocked by CETP and LCAT inhibitors. In a group of particles with such a complex biology as HDL, knowledge of the interaction between apo-lipoproteins, lipids and enzymes is key for an increased understanding of the yet multiple unknown features of its function. Solving the HDL paradox will necessitate the development of techniques to explore HDL function that are practical and well adapted to clinical studies and eventually become useful in patient monitoring. The confluence of proteomic, functional studies, HDL subclasses, PON1 assays and zymogram will yield data to draw a more elaborate and comprehensive picture of the function of HDL. It must be noted that all these studies are static and conducted in the fasting state. The crucial phase will be achieved when human kinetic studies (both in the fasting and post-prandial states) on HDL-PON1, apoA-I and lipid fate in the circulation are carried out.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Clinica Chimica Acta - Volume 439, 15 January 2015, Pages 5-13
Journal: Clinica Chimica Acta - Volume 439, 15 January 2015, Pages 5-13
نویسندگان
Alejandro Gugliucci, Teresita Menini,