2026-05-22T00:46:52Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/79492024-09-27T09:40:44Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605

00925njm 22002777a 4500 dc Hamczyk, Magda R. author Villa-Bellosta, Ricardo author Andres, Vicente author 2015 The key roles of macrophages in atherosclerosis include the phagocytosis of apoptotic and necrotic cells and cell debris, whose accumulation in atherosclerotic lesions exacerbates inflammation and promotes plaque vulnerability. Evidence is accumulating that macrophage phagocytic functions peak at the early stages of atherosclerosis and that the reduced phagocytosis at the late stages of disease leads to the generation of necrotic cores and a defective resolution of inflammation, which in turn promotes plaque rupture, thrombus formation, and life-threatening acute ischemic events (myocardial infarction and stroke). The impaired resolution of inflammation in advanced lesions featuring loss of macrophage phagocytic activity may be in part due to an imbalance between M1 and M2 subsets of polarized macrophages. A better understanding of the mechanisms that regulate macrophage phagocytic activity in the context of atherosclerosis may therefore help identify novel therapeutic targets. This chapter presents a protocol for establishing primary mouse macrophage cultures, a method for polarizing macrophages to the M1 and M2 states, and a method for the in vitro study of macrophage phagocytosis of IgG-opsonized or IgM/complement component 3-opsonized erythrocytes. Methods Mol Biol. 2015; 1339:235-46 10.1007/978-1-4939-2929-0_16 1940-6029 978-1-4939-2928-3 1064-3745 Methods in molecular biology (Clifton, N.J.) 26445793 http://hdl.handle.net/20.500.12105/7949 Complement component 3 IgG IgM Macrophage Opsonization Phagocytosis Red blood cells In Vitro Macrophage Phagocytosis Assay