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Atherosclerosis: Difference between revisions
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→Endothelial cells
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The endothelium produces antithrombotic molecules in order to prevent blood from clotting. Certain molecules such as heparin sulfate, thrombomodulin, and plasminogen rest on the endothelial surface whereas molecules such as prostacyclin and nitric oxide (NO) enter the blood. Endothelium can produce prothrombotic molecules when it encounters stressors; however, it normally maintains a balanced anticoagulant state, maintaining blood fluidity.<br /> | The endothelium produces antithrombotic molecules in order to prevent blood from clotting. Certain molecules such as heparin sulfate, thrombomodulin, and plasminogen rest on the endothelial surface whereas molecules such as prostacyclin and nitric oxide (NO) enter the blood. Endothelium can produce prothrombotic molecules when it encounters stressors; however, it normally maintains a balanced anticoagulant state, maintaining blood fluidity.<br /> | ||
Endothelial cells also have an important function as a regulator of the immune response. In a normal situation without pathologic stimuli, endothelial cells are not capable to | Endothelial cells also have an important function as a regulator of the immune response. In a normal situation without pathologic stimuli, endothelial cells are not capable to attract and bind patrolling leukocytes, thus maintaining an anti-inflammatory state. When local injury or infection initiates pathologic stimulation, endothelial cells respond by secreting chemokines that attract white blood cells to the injured area. Additionally, endothelium produces cell surface adhesion molecules, which recruit mononuclear cells to the endothelium and therefore promote their migration to the injury site. This response is important for the development of atherosclerosis.<br /> | ||
Another function of endothelium is to modulate contraction of smooth muscle cells in the media by releasing substances such as vasodilators and vasoconstrictors. Vasodilators (e.g. NO, prostacyclin) and vasoconstrictors (e.g. endothelin) fine-tune the resistance of the vessel and subsequently alter the arterial blood flow. Endothelium normally maintains a state of net relaxed vasomotor tone with | Another function of endothelium is to modulate contraction of smooth muscle cells in the media by releasing substances such as vasodilators and vasoconstrictors. Vasodilators (e.g. NO, prostacyclin) and vasoconstrictors (e.g. endothelin) fine-tune the resistance of the vessel and subsequently alter the arterial blood flow. Endothelium normally maintains a state of net relaxed vasomotor tone with a predominance of vasodilators. Endothelium can also respond to various physical stimuli such as shear stress and can additionally dilate the blood vessel. The endothelium principally regulates such response through release of NO. This endothelial-dependent response is called flow-mediated vasodilation (FMD), which can be measured for clinical evaluation of endothelial function. For example, impairment of FMD is observed in the early stages of atherosclerosis. However, endothelial function tests are currently not recommended to be used for surrogate markers in clinical practice since the tests are technically challenging and the validation of clinical benefits in the evaluation of cardiovascular risk requires more evidence.<br /> | ||
As mentioned earlier, endothelial cells can respond to or in other words get ‘activated’ due to changes in the local extracellular milieu. Examples of such changes are common stresses (e.g. shear stress and mild changes in temperature), transient infections and minor trauma. The term ‘endothelial cell activation’ (EC activation) refers to a change from the normal state, illustrated by loss of barrier function, pro-adhesive (leukocyte adhesion), vasoconstriction, and procoagulant properties. EC activation is not necessarily linked to disease and can be temporary and mild or permanent and severe.<br /> | As mentioned earlier, endothelial cells can respond to or in other words get ‘activated’ due to changes in the local extracellular milieu. Examples of such changes are common stresses (e.g. shear stress and mild changes in temperature), transient infections and minor trauma. The term ‘endothelial cell activation’ (EC activation) refers to a change from the normal state, illustrated by loss of barrier function, pro-adhesive (leukocyte adhesion), vasoconstriction, and procoagulant properties. EC activation is not necessarily linked to disease and can be temporary and mild or permanent and severe.<br /> | ||