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Artículo

Apolipoprotein A-I Helsinki promotes intracellular acyl-CoA cholesterol acyltransferase (ACAT) protein accumulation

Toledo, Juan Domingo; Garda, Horacio AlbertoIcon ; Cabaleiro, Laura VirginiaIcon ; Cuellar, Angela; Pellon Maison, MagaliIcon ; Gonzalez Baro, Maria del RosarioIcon ; Gonzalez, Marina CeciliaIcon
Fecha de publicación: 05/2013
Editorial: Springer
Revista: Molecular and Cellular Biochemistry
ISSN: 0300-8177
Idioma: Inglés
Tipo de recurso: Artículo publicado
Clasificación temática:
Bioquímica y Biología Molecular

Resumen

Reverse cholesterol transport is a process of high antiatherogenic relevance in which apolipoprotein AI (apoA-I) plays an important role. The interaction of apoA-I with peripheral cells produces through mechanisms that are still poorly understood the mobilization of intracellular cholesterol depots toward plasma membrane. In macrophages, these mechanisms seem to be related to the modulation of the activity of acyl-CoA cholesterol acyltransferase (ACAT), the enzyme responsible for the intracellular cholesterol ester biosynthesis that is stored in lipid droplets. The activation of ACAT and the accumulation of lipid droplets play a key role in the transformation of macrophages into foam cells, leading to the formation of atheroma or atherosclerotic plaque. ApoA-I Helsinki (or DK107) is a natural apoA-I variant with a lysine deletion in the central protein region, carriers of which have increased atherosclerosis risk. We herein show that treatment of cultured RAW macrophages or CHOK1 cells with DK107, but not with wild-type apoA-I or a variant containing a similar deletion at the C-terminal region (DK226), lead to a marked increase (more than 10 times) in the intracellular ACAT1 protein level as detected by western blot analysis. However, we could only detect a slight increase in cholesteryl ester produced by DK107 mainly when Chol loading was supplied by low-density lipoprotein (LDL). Although a similar choline-phospholipid efflux is evoked by these apoA-I variants, the change in phosphatidylcholine/ sphyngomyelin distribution produced by wild-type apoA-I is not observed with either DK107 or DK226.
Palabras clave: Acyl Coa-Cholesterol Acyl Transferase , Cholesterol Efflux , Phospholipid Efflux , Murine Macrophages
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info:eu-repo/semantics/restrictedAccess Excepto donde se diga explícitamente, este item se publica bajo la siguiente descripción: Creative Commons Attribution-NonCommercial-ShareAlike 2.5 Unported (CC BY-NC-SA 2.5)
Identificadores
URI: http://hdl.handle.net/11336/24112
DOI: http://dx.doi.org/10.1007/s11010-013-1585-y
URL: https://link.springer.com/article/10.1007%2Fs11010-013-1585-y
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Articulos(INIBIOLP)
Articulos de INST.DE INVEST.BIOQUIMICAS DE LA PLATA
Citación
Toledo, Juan Domingo; Garda, Horacio Alberto; Cabaleiro, Laura Virginia; Cuellar, Angela; Pellon Maison, Magali; et al.; Apolipoprotein A-I Helsinki promotes intracellular acyl-CoA cholesterol acyltransferase (ACAT) protein accumulation; Springer; Molecular and Cellular Biochemistry; 377; 1-2; 5-2013; 197-205
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