Financiado en parte por Amarin Corporation, Amarin Pharma
Eicosapentaenoic acid reduces membrane fluidity, inhibits cholesterol domain formation, and normalizes bilayer width in atherosclerotic-like model membranes
Mason RP, Jacob RF, Shrivastava S, Sherratt SCR, Chattopadhyay A
Biochimica et biophysica acta · 129 citas
Etiquetas de revisión
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Cómo se estudió
- Diseño
- Estudio in vitro o de mecanismos (clasificado por nuestro filtro de IA)
- Estudiado en
- Células o muestras de laboratorio
- Resultado principal
- Solo mecanismos
Quién lo pagó
- Financiación
- Financiado por la industria
- Empresa
- Amarin Corporation
- Gobierno
- Department of Science and Technology, Ministry of Science and Technology, India
- Gobierno
- Council of Scientific and Industrial Research, India
- Empresa
- Amarin Pharma
Según 4 financiadores declarados.
Publicación
- Publicado
- 2016-10-09 · Biochim Biophys Acta · vol. 1858 · número 12 · págs. 3131–3140
- Editorial
- Elsevier BV
- Citado
- 177 citas · más que el 98% de estudios similares · 7.7× el promedio de su campo
- Impacto
- Entre el 10 % más citado de su campo
- Referencias
- 76 trabajos
- Acceso
- Acceso abierto (revista híbrida) · CC-BY
- Áreas de investigación
- Fatty Acid Research and Health · Cholesterol and Lipid Metabolism · Lipid metabolism and biosynthesis
- Palabras clave
- Bilayer, Eicosapentaenoic acid, Membrane, Membrane fluidity, Lipid bilayer, Cholesterol, Biophysics, Chemistry, Internal medicine, Materials science, Medicine, Biochemistry, Fatty acid, Biology, Polyunsaturated fatty acid
- MeSH
- humans, cholesterol, docosahexaenoic acids, eicosapentaenoic acid, lipid bilayers, membrane fluidity, dose-response relationship, drug, atherosclerosis
5 autores
- Richard Preston Mason🇺🇸 · autor de correspondenciaBrigham and Women's Hospital; Harvard University
- Robert Francis Jacob
- Sandeep Kumar Shrivastava🇮🇳Centre for Cellular and Molecular Biology
- Samuel C. R. Sherratt
- Amitabha Chattopadhyay🇮🇳Centre for Cellular and Molecular Biology
Resumen
El texto original del estudio, en el idioma en que se publicó.
Cholesterol crystalline domains characterize atherosclerotic membranes, altering vascular signaling and function. Omega-3 fatty acids reduce membrane lipid peroxidation and subsequent cholesterol domain formation. We evaluated non-peroxidation-mediated effects of eicosapentaenoic acid (EPA), other TG-lowering agents, docosahexaenoic acid (DHA), and other long-chain fatty acids on membrane fluidity, bilayer width, and cholesterol domain formation in model membranes. In membranes prepared at 1.5:1 cholesterol-to-phospholipid (C/P) mole ratio (creating pre-existing domains), EPA, glycyrrhizin, arachidonic acid, and alpha linolenic acid promoted the greatest reductions in cholesterol domains (by 65.5%, 54.9%, 46.8%, and 45.2%, respectively) compared to controls; other treatments had modest effects. EPA effects on cholesterol domain formation were dose-dependent. In membranes with 1:1 C/P (predisposing domain formation), DHA, but not EPA, dose-dependently increased membrane fluidity. DHA also induced cholesterol domain formation without affecting temperature-induced changes in-bilayer unit cell periodicity relative to controls (d-space; 57Å-55Å over 15-30°C). Together, these data suggest simultaneous formation of distinct cholesterol-rich ordered domains and cholesterol-poor disordered domains in the presence of DHA. By contrast, EPA had no effect on cholesterol domain formation and produced larger d-space values relative to controls (60Å-57Å; p<0.05) over the same temperature range, suggesting a more uniform maintenance of lipid dynamics despite the presence of cholesterol. These data indicate that EPA and DHA had different effects on membrane bilayer width, membrane fluidity, and cholesterol crystalline domain formation; suggesting omega-3 fatty acids with differing chain length or unsaturation may differentially influence membrane lipid dynamics and structural organization as a result of distinct phospholipid/sterol interactions.
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