How do monocytes affect atherosclerosis?
How do monocytes affect atherosclerosis?
During the development and exacerbation of atherosclerosis, monocytes infiltrate the vessel wall and become lesional macrophages. Macrophages ingest oxidized lipoproteins via scavenger receptors and, as lipid-rich foam cells, contribute to the physical bulk of developing plaques.
Are monocytes involved in atherosclerosis?
In addition to the accumulation of lipids and formation of atherogenic ‘foam’ cells, monocytes may promote atherosclerotic plaque growth by production of inflammatory cytokines, matrix metalloproteinases, and reactive oxidative species.
Are macrophages involved in atherosclerosis?
Macrophages in atherosclerotic lesions actively participate in lipoprotein ingestion and accumulation giving rise to foam cells filled with lipid droplets. Accumulation of foam cells contributes to lipid storage and atherosclerotic plaque growth.
What is the role of macrophages in atherosclerosis?
Macrophages in atherosclerotic cardiovascular disease play a central role in the development of plaques. Classically activated M1 macrophages are implicated in initiating and sustaining inflammation, and alternatively activated or M2 macrophages are linked to inflammation resolution.
What cytokines do macrophages release?
When macrophages are exposed to inflammatory stimuli, they secrete cytokines such as tumor necrosis factor (TNF), IL-1, IL-6, IL-8, and IL-12. Although monocytes and macrophages are the main sources of these cytokines, they are also produced by activated lymphocytes, endothelial cells, and fibroblasts.
What is a macrophage?
macrophage, type of white blood cell that helps eliminate foreign substances by engulfing foreign materials and initiating an immune response. Macrophages are constituents of the reticuloendothelial system (or mononuclear phagocyte system) and occur in almost all tissues of the body.
Why do macrophages take up LDL?
In this receptor-independent uptake process, macrophages take up LDL as part of the fluid that they ingest by these pinocytosis pathways. This produces cholesterol accumulation in macrophages to levels characteristic of macrophage foam cells in atherosclerotic plaques.
What do macrophages do?
Macrophages are effector cells of the innate immune system that phagocytose bacteria and secrete both pro-inflammatory and antimicrobial mediators. In addition, macrophages play an important role in eliminating diseased and damaged cells through their programmed cell death.
Are macrophages monocytes?
Monocytes and macrophages are members of the mononuclear phagocyte system, a component of innate immunity. Monocytes are bone marrow derived leukocytes that circulate in the blood and spleen. Once recruited to tissues, monocytes are capable of differentiating into macrophages and dendritic cells.
Are macrophages good or bad?
Macrophages play a central role in guiding proper organ and tissue development, physiological healing, and in maintaining tissue homeostasis. Further, they are one of the major cell components of the inflammatory response.
What is the role of macrophage in immune response?
How are monocytes and macrophages involved in atherosclerosis?
Monocytes and their descendant macrophages are essential to the development and exacerbation of atherosclerosis, a lipid-driven inflammatory disease. Lipid-laden macrophages, known as foam cells, reside in early lesions and advanced atheromata.
What happens to ly-6c high monocytes as disease worsens?
As disease worsens, the number of Ly-6C high monocytes in the blood rises. 12 – 14 A large body of evidence shows that in addition to increasing in number, Ly-6C high monocytes preferentially adhere to activated endothelium, infiltrate the vessel wall, and become lesional macrophages.
How are myeloid cells involved in atherosclerosis?
Myeloid cells are key cellular protagonists of the inflammatory response that drives atherogenesis. 2, 3 Circulating monocytes adhere to the activated endothelium, infiltrate the vessel wall, become lesional macrophages, and participate decisively in the development and exacerbation of atherosclerosis.
How are macrophages and endothelial cells related?
By co-culturing macrophages and endothelial cells with miR-92a overexpression or knockdown, the investigators demonstrated that endothelial cells can promote the atheroprone phenotypes of macrophages through miR-92a.
