Case Study Of Atherosclerosis

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Chapter 1
Atherosclerosis

Structure of the normal artery:

Cell types composing the normal artery:
Endothelial Cells:
The endothelial cell (EC) of the arterial intima constitutes an important contact surface with blood. It plays an important role in vascular homeostasis. This blood compatibility is due to presences of heparan sulfate proteoglycan molecules on the surface of the EC. These molecules can serve as a cofactor for antithrombin III, which inhibit thrombin. The surface of the EC also contains thrombomodulin which activates protein C and S. Also the EC can produce tissue- and urokinase- type plasminogen activators which activate plasminogen into plasmin.(Fig.1) ECs are originated from a common origin known as blood islands in the
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Then oxidation of lipoproteins occur. The modified lipoproteins will induce local cytokines production. These cytokines then induce expression of adhesion molecules. There are several adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) or CD106, intercellular adhesion molecule 1 (ICAM-1) and selectins including E-selectin or CD62E and P-selectin or CD62P.3,4,5,6 Leukocyte accumulation occurs early in lesion generation. Once adherent to ECs ,they receive a signal from the chemoatractant cytokines or chemokines to penetrate the endothelial monolayer. Chemokines include monocytes chemoatractant protein 1 (MCP-1) or CCL2 and lymphocyte selective cytokines (IP-10 or CXCL10, I-TAC or CXCL11 and MIG or CXCL9). Macrophages are retained in the intimal layer by a protein called netrin-1 interacting with its receptor UNC5b.7,8
Intracellular lipid accumulation
The monocytes once reached the arterial intimal layer, can accumulate lipid particles to be transformed into foam cells or lipid laden macrophages as they exhibit scavenger receptors for modified
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It depends on formation large number of antigen receptors. The antigen presenting cells include the macrophages, dendritic cells and ECs. They allow the antigens to activate T-cells. The activated T cells then secrete great amount of cytokines that modulate atherogenesis. The T helper cells are divided into two types. T helper 1 subtype (Th1) that secrete proinflammatory cytokines that lead to plaque destabilization. Th2 cells produce cytokines that can inhibit inflammation. Cytolytic T cells express cytotoxic factors that can promote apoptosis of SMCs, ECs and macrophages. Death of these cells occur in the atherosclerotic lesion and may lead to plaque progression and complications. Regulatory T cells (Tregs) produce transforming growth factor –beta (TGF-β) and interleukin-10 which have anti-inflammatory action. B1 cells produce antibodies which can protect against atherosclerosis in vivo while B2 cells promote atherosclerosis by activating proinflammatory

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