Endothelial cells line all blood vessels, thus providing an interface between the blood and vascular smooth muscle. Once thought to be a passive diffusion barrier, these cells are recognized as a dynamic participant in regulation of blood pressure, clotting of the blood and responses to injury and infection. Endothelial cells secrete chemicals called cytokines and gases like nitric oxide (NO) into the blood and toward the cells of the blood vessel wall (smooth muscle, nerve endings).
In health, these chemicals when secreted from the endothelium into the blood prevent formation of unwanted blood clots and direct white blood cells to sights of vascular injury and infection. When secreted toward smooth muscle cells, these chemicals influence contraction, proliferation, and migration of these cells thus affecting blood pressure and repair. Experiments in our laboratory are focused toward understanding what happens to these cells in the absence of estrogen and in the presence of infection to cause blood clots, high blood pressure and atherosclerosis.
How does estrogen alter the vascular response to injury? Estrogen and other hormones affect all cells of the blood vessel wall (down-stream response) and cells of the blood like platelets (up-stream response). Platelets release many types of chemicals, which cause formation of blood clots and growth, migration and differentiation of cells in the blood vessels. Estrogen affects production of these factors in bone marrow megakaryocytes, the precursors of platelets. (Abbreviations: ADP, ATP: adenosine di- tri- phosphate; 5-HT: 5-hydroxytryptamine; PDGF: platelet derived growth factor; PGI2: prostacyclin; TBA2: thromboxane; TGF β: transforming growth factor β; VEGF: vascular endothelial growth factor).
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