Endothelial cell repair

Inhibits VSMC mitogens and matrix formation Stimulates endothelial cell repair Stimulates arterial endothelial cell PGI2 synthesis Facilitates metabolism of triglyceride rich lipoproteins Faciliates fibrinolysis... 

Although mast cells and basophils probably account for >90% of stored histamine in the body, histamine is also present in platelets, enterochromaffin-like cells, endothelial cells, and neurons. Histamine can act as a neurotransmitter in the brain. Histaminergic nerves have their cell bodies within a very small area of the brain (the magnocellular nuclei of the posterior hypothalamus) but have axons in most areas of the forebrain. There is also evidence for axons projecting into the spinal (Fig. 1) cord. Finally, there is evidence that histamine synthesis can be induced in tissues undergoing rapid tissue growth and repair. In certain neonatal tissues (e.g. liver), the rate of synthesis of this unstored diffusable histamine (termed nascent histamine) is profound and may point to a role for histamine is cell proliferation. 

Growth factor facilitates vascular endothelial cell, vascular smooth muscle cell, and fibroblast multiplication and growth, leading to repair of damaged blood vessels. 

The wound assay [49] is another method of measuring endothelial cell migration. This assay is based on damaging or wounding a confluent monolayer of endothelial cells and the subsequent repair or closing of the wound by migration of endothelial cells. This assay can be carried out using different matrix components. 

The field of stem cell therapy has benefited from the work of numerous basic and clinical scientists whose studies have greatly improved our understanding of the processes involved in cardiac repair and neovascularization. The creation of new blood vessels (neovascularization) requires the formation of new mature endothelial cells. In this process, the new... 

To maintain hemostasis, blood must be retained in the vasculature as fluid. At the same time, blood components must be able to respond rapidly with a clot when a vascular injury occurs. To repair a vascular injury, platelets in blood first adhere as aggregates to the endothelial cells at the affected site and form an initial blood clot. Platelets then stimulate and activate coagulation factors found in plasma to form a more stable fibrin clot. As the injury is resolved and healed, the clot is degraded. Thrombosis is a pathological event wherein a blood clot occludes a blood vessel, resulting in ischemic necrosis of the tissue fed by the blood vessel. Ischemic necrosis involves local anemia and oxygen deprivation. Thrombosis of a coronary artery may lead to myocardial infarction or unstable angina [20]. 

The literature is rich with examples of metal-nitrosyl complexes, and it would be surprising if the generation of NO by the immune system did not result in the formation of many such adducts. Previous articles have presented summaries of metal proteins that form NO complexes (Butler et al., 1985 Henry et al., 1993), and more recently evidence has mounted that generation of NO by the immune system and by endothelial cells produces a variety of iron-nitrosyl complexes (Mulsch et al., 1993 Vanin et al., 1993 Lancaster et al., 1994). It is unclear which of the potential products will prove to be of physiological relevance, but because the enzymes that may be involved range from the central focus of oxidative cellular metabolism (LoBrutto et al., 1983) to the enzymes of DNA repair (Asahara et al., 1989), the list of potential targets is long and varied. 

Lewis, J.G. Swenberg, J.A. (1983) The kinetics of DNA alkylation, repair and replication in hepatocytes, Kupffer cells, and sinusoidal endothelial cells in rat liver during continuous exposure to 1,2-dimethylhydrazine. Carcinogenesis, 4, 529-536... 

Oxidised LDL in the artery wall initiates a series of reactions designed to repair the damage it causes. Initial damage triggers an inflammatory response. Monocytes enter the artery waU from the bloodstream, with platelets adhering to the area of insult. This may be promoted by induction of factors such as vascular ceU adhesion molecule 1 (VCAM-1), a cell-surface sialoglycoprotein that is expressed by cytokine-activated endothelium. This membrane protein mediates leukocyte-endothelial cell adhesion and signal transduction, and may play a role in the development of atherosclerosis and rheumatoid arthritis. 

In other studies, we also showed that resveratrol effectively suppressed proliferation of cultured bovine pulmonary aortic endothelial cells (BPAEC). These results imply that resveratrol, delivered to endothelial cells in sufficient concentrations to inhibit proliferation in vivo, could facilitate rapid and efficient repair of damages on the endothelium, with the overall effect of decreasing the probability of sustained endothelial injury and exposure of the subendothelial matrix, which would trigger the formation of atherosclerotic plaques and the development of... 

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