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Multifunctional roles of macrophages in the development and progression of atherosclerosis in humans and experimental animals.
Med Electron Microsc. 2002 Dec; 35(4):179-203.ME

Abstract

In atherosclerosis, macrophages are important for intracellular lipid accumulation and foam cell formation. Monocytes respond to chemotactic factors, cytokines, and macrophage growth factors produced by vascular endothelial cells, smooth muscle cells, and infiltrated cells, by migrating from peripheral blood into the arterial intima and differentiating into macrophages in atherosclerotic lesions. Although various chemotactic factors are known to induce monocyte migration, monocyte chemoattractant protein-1 is the most important and powerful inducer of migration into atherosclerotic lesions. Macrophage colony-stimulating factor is crucial for monocyte/macrophage differentiation and proliferation, and for the survival of macrophages in these lesions. A minor population of macrophages can proliferate in the atherosclerotic lesions themselves, particularly in the early stage. The macrophages express a variety of receptors, particularly scavenger receptors, and take up modified lipoproteins, including oxidized low-density lipoprotein, beta-very-low-density lipoprotein, and/or enzymatically degraded low-density lipoprotein. These cells accumulate cholesterol esters in the cytoplasm, which leads to foam cell formation in lesion development. Among various scavenger receptors, class A type I and type II macrophage scavenger receptors (MSR-A I,II) play the most important role in the uptake of oxidized low-density lipoprotein by macrophages. In addition, macrophages and macrophage-derived foam cells produce ceroid and advanced glycation end-products (AGEs) and accumulate these substances in their cytoplasm. Extracellularly generated AGEs are taken up by macrophages via receptors for AGEs, including MSR-AI,II. Most foam cells die in loco because of apoptosis, and some foam cells escape from the lesions into peripheral blood. Macrophages also play multifaceted roles in inducing plaque rupture, blood coagulation, and fibrinolysis via the production of various enzymes, activators, inhibitors, and bioactive mediators. During the development of atherosclerosis, macrophages interact with vascular endothelial cells, medial smooth muscle cells, and infiltrated inflammatory cells, particularly T cells and dendritic cells. This review, based on data accumulated in studies of atherosclerosis in humans and experimental animals, focuses on the multifunctional roles of macrophages in the pathogenesis and progression of atherosclerosis.

Authors+Show Affiliations

Fuji Bio Co Ltd, 1-14-23 Kasuga, Kumamoto 860-0047, Japan. fujibaio@orange.ocn.ne.jpNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

12658354

Citation

Takahashi, Kiyoshi, et al. "Multifunctional Roles of Macrophages in the Development and Progression of Atherosclerosis in Humans and Experimental Animals." Medical Electron Microscopy : Official Journal of the Clinical Electron Microscopy Society of Japan, vol. 35, no. 4, 2002, pp. 179-203.
Takahashi K, Takeya M, Sakashita N. Multifunctional roles of macrophages in the development and progression of atherosclerosis in humans and experimental animals. Med Electron Microsc. 2002;35(4):179-203.
Takahashi, K., Takeya, M., & Sakashita, N. (2002). Multifunctional roles of macrophages in the development and progression of atherosclerosis in humans and experimental animals. Medical Electron Microscopy : Official Journal of the Clinical Electron Microscopy Society of Japan, 35(4), 179-203.
Takahashi K, Takeya M, Sakashita N. Multifunctional Roles of Macrophages in the Development and Progression of Atherosclerosis in Humans and Experimental Animals. Med Electron Microsc. 2002;35(4):179-203. PubMed PMID: 12658354.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Multifunctional roles of macrophages in the development and progression of atherosclerosis in humans and experimental animals. AU - Takahashi,Kiyoshi, AU - Takeya,Motohiro, AU - Sakashita,Naomi, PY - 2003/3/27/pubmed PY - 2003/7/3/medline PY - 2003/3/27/entrez SP - 179 EP - 203 JF - Medical electron microscopy : official journal of the Clinical Electron Microscopy Society of Japan JO - Med Electron Microsc VL - 35 IS - 4 N2 - In atherosclerosis, macrophages are important for intracellular lipid accumulation and foam cell formation. Monocytes respond to chemotactic factors, cytokines, and macrophage growth factors produced by vascular endothelial cells, smooth muscle cells, and infiltrated cells, by migrating from peripheral blood into the arterial intima and differentiating into macrophages in atherosclerotic lesions. Although various chemotactic factors are known to induce monocyte migration, monocyte chemoattractant protein-1 is the most important and powerful inducer of migration into atherosclerotic lesions. Macrophage colony-stimulating factor is crucial for monocyte/macrophage differentiation and proliferation, and for the survival of macrophages in these lesions. A minor population of macrophages can proliferate in the atherosclerotic lesions themselves, particularly in the early stage. The macrophages express a variety of receptors, particularly scavenger receptors, and take up modified lipoproteins, including oxidized low-density lipoprotein, beta-very-low-density lipoprotein, and/or enzymatically degraded low-density lipoprotein. These cells accumulate cholesterol esters in the cytoplasm, which leads to foam cell formation in lesion development. Among various scavenger receptors, class A type I and type II macrophage scavenger receptors (MSR-A I,II) play the most important role in the uptake of oxidized low-density lipoprotein by macrophages. In addition, macrophages and macrophage-derived foam cells produce ceroid and advanced glycation end-products (AGEs) and accumulate these substances in their cytoplasm. Extracellularly generated AGEs are taken up by macrophages via receptors for AGEs, including MSR-AI,II. Most foam cells die in loco because of apoptosis, and some foam cells escape from the lesions into peripheral blood. Macrophages also play multifaceted roles in inducing plaque rupture, blood coagulation, and fibrinolysis via the production of various enzymes, activators, inhibitors, and bioactive mediators. During the development of atherosclerosis, macrophages interact with vascular endothelial cells, medial smooth muscle cells, and infiltrated inflammatory cells, particularly T cells and dendritic cells. This review, based on data accumulated in studies of atherosclerosis in humans and experimental animals, focuses on the multifunctional roles of macrophages in the pathogenesis and progression of atherosclerosis. SN - 0918-4287 UR - https://www.unboundmedicine.com/medline/citation/12658354/Multifunctional_roles_of_macrophages_in_the_development_and_progression_of_atherosclerosis_in_humans_and_experimental_animals_ L2 - https://dx.doi.org/10.1007/s007950200023 DB - PRIME DP - Unbound Medicine ER -