Fisiologia

ARTICULO CIENTIFICO #1
Curr Opin Lipidol. 2011 Oct;22(5):386-93.

Receptor-independent fluid-phase pinocytosis mechanisms for induction of foam cell formation with native low-density lipoproteinparticles.

Kruth HS.

Source
Section of Experimental Atherosclerosis, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland 20892-1422, USA. kruthh@nhibi.nih.gov
Abstract
PURPOSEOF REVIEW:
Because early findings indicated that native low-density lipoprotein (LDL) did not substantially increase macrophage cholesterol content during in-vitro incubations, investigatorspresumed that LDL must be modified in some way to trigger its uptake by the macrophage. The purpose of this review is to discuss recent findings showing that native unmodified LDL can induce massivemacrophage cholesterol accumulation mimicking macrophage foam cell formation that occurs within atherosclerotic plaques.
RECENT FINDINGS:
Macrophages that show high rates of fluid-phase pinocytosisalso show similar high rates of uptake of native unmodified LDL through nonreceptor mediated uptake within both macropinosomes and micropinosomes. Nonsaturable fluid-phase uptake of LDL by macrophagesconverts the macrophages into foam cells. Different macrophage phenotypes demonstrate either constitutive fluid-phase pinocytosis or inducible fluid-phase pinocytosis. Fluid-phase pinocytosis has beendemonstrated by macrophages within mouse atherosclerotic plaques indicating that this pathway contributes to plaque macrophage cholesterol accumulation.
SUMMARY:
Contrary to what has beenbelieved previously, macrophages can take up large amounts of native unmodified LDL by receptor-independent, fluid-phase pinocytosis converting these macrophages into foam cells. Thus, targeting macrophagefluid-phase pinocytosis should be considered when investigating strategies to limit macrophage cholesterol accumulation in atherosclerotic plaques.

PMID:

21881499

[PubMed - in process]...