PubMed · 13226675
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P CHICHE. 1954. [Hypercoagulability syndrome].. https://pubmed.ncbi.nlm.nih.gov/13226675/
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Thrombin signaling in the endothelium is linked to multiple phenotypic changes, including alterations in permeability, vasomotor tone, and leukocyte trafficking. The thrombin signal is transduced, at least in part, at the level of gene transcription. In this review, we focus on the role of thrombin signaling and transcriptional networks in mediating downstream gene expression and endothelial phenotype. In addition, we report the results of DNA microarrays in control and thrombin-treated endothelial cells. We conclude that (1) thrombin induces the upregulation and downregulation of multiple genes in the endothelium, (2) thrombin-mediated gene expression involves a multitude of transcription factors, and (3) future breakthroughs in the field will depend on a better understanding of the spatial and temporal dynamics of these transcriptional networks.
In this work we demonstrate that the unstable trigger waves, connecting stable and unstable spatially uniform steady states, can create intricate dynamic regimes in one-dimensional three-component reaction-diffusion model describing blood clotting. Among the most interesting regimes are the composite and replicating waves running at a constant velocity. The front part of the running composite wave remains constant, while its rear part oscillates in a complex manner. The rear part of the running replicating wave periodically gives rise to new daughter waves, which propagate in the direction opposite the parent wave. The domain of these intricate regimes in parameter space lies in the region of monostability near the region of bistability.
There are several potential mechanisms by which HDLs protect against the development of vascular disease. One relates to the unique ability of these lipoproteins to remove cholesterol from the arterial wall. Another is the ability of HDL to prevent and eventually correct endothelial dysfunction, a key variable in the pathogenesis of atherosclerosis and its complications. HDLs help maintain endothelial integrity, facilitate vascular relaxation, inhibit blood cell adhesion to vascular endothelium, reduce platelet aggregability and coagulation, and may favor fibrinolysis. These functions of HDLs complement their activity in arterial cholesterol removal by providing an excellent rationale for favorably influencing pathological processes underlying a variety of clinical conditions, such as accelerated atherosclerosis, acute coronary syndromes, and restenosis after coronary angioplasty, through a chronic or acute elevation of plasma HDL concentration.