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Acta Biochimica et Biophysica Sinica Advance Access originally published online on July 27, 2009
Acta Biochimica et Biophysica Sinica 2009 41(9):773-780; doi:10.1093/abbs/gmp066
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© The Author 2009. Published by ABBS Editorial Office in association with Oxford University Press on behalf of the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences.

Macropinocytosis contributes to the macrophage foam cell formation in RAW264.7 cells

Wenqi Yao{dagger}, Ke Li{dagger} and Kan Liao*

State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China

* Correspondence address. Tel: +86-21-54921113; Fax: +86-21-54921011; E-mail: kliao{at}sibs.ac.cn


  Abstract

The key event in the atherosclerosis development is the lipids uptake by macrophage and the formation of foam cell in subendothelial arterial space. Besides the uptake of modified low-density lipoprotein (LDL) by scavenger receptor-mediated endocytosis, macrophages possess constitutive macropinocytosis, which is capable of taking up a large quantity of solute. Macrophage foam cell formation could be induced in RAW264.7 cells by increasing the serum concentration in the culture medium. Foam cell formation induced by serum could be blocked by phosphoinositide 3-kinase inhibitor, LY294002 or wortmannin, which inhibited macropinocytosis but not receptor-mediated endocytosis. Further analysis indicated that macropinocytosis took place at the gangliosides-enriched membrane area. Cholesterol depletion by β-methylcyclodextrin-blocked macropinocytosis without affecting scavenger receptor-mediated endocytosis of modified LDLs. These results suggested that macropinocytosis might be one of the important mechanisms for lipid uptake in macrophage. And it made significant contribution to the lipid accumulation and foam cell formation.

Keywords    macrophage; macropinocytosis; foam cell; PI3-kinase; atherosclerosis

Received: April 10, 2009; Accepted: May 18, 2009

{dagger} These authors contributed equally to this work.


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