Cellular and Molecular Basis of Human Biology
Lawrence S. Chan, William C. Tang in Engineering-Medicine, 2019
Many cells in the human body are stationary in nature, that means that they stay in certain body location all their lives. Major stationary cells include the followings: Epithelial cells (of the skin, mucous membranes, hair follicles, cornea, retina, and lining of esophagus, intestines, and bladders).Fibroblasts (cells that produce many extracellular matrices like collagens).Melanocytes (pigment-producing cells of skin, mucous membrane, retina, and iris).Endothelial cells (of the lining of blood or lymphatic vessels).Neurons (of the nerve and brain).Muscle cells (cells that constitute the muscle mass).Bone-building cells (osteoblasts).Bone-breakdown cells (osteoclasts), and many more.
Endothelial Cells and Hemodynamics
Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos in McDonald's Blood Flow in Arteries, 2022
Endothelial cell dysfunction triggered by different stimuli perturbs the hemostasis-mediating balance between procoagulant and anticoagulant factors. Inflammation and endothelial cell dysfunction are directly related to all stages of atherosclerosis, thrombosis and related complications (Bergan et al., 2006; Chiu et al., 2009; Dimmeler et al., 2002; Garin and Berk, 2006; Gimbrone, 1995; Ross and Glomset, 1976; Topper and Gimbrone Jr., 1999). The permeability and thus the function of damaged/dysfunctional endothelium is significantly altered as the dysfunctional endothelial cell layer is activated by cardiovascular risk factors (Libby et al., 2010). Intercellular junctions (identified primarily as tight, gap and adherence junctions), the most important regulators of endothelium integrity and permeability, are modulated by several biological factors including inflammatory mediators (Bordron et al., 1998; Khazaei and Nematbakhsh, 2004). Consequently, transportation of macromolecules through endothelial junctions is significantly altered in response to inflammatory mediators, increasing their permeability (Lum and Malik, 1994, 1996). Increased permeability opens the gateway to lipoproteins, monocytes and macrophages, triggering smooth muscle cell migration and proliferation (Celermajer, 1997) and promoting an atherosclerotic plaque initiation and progression (Davignon and Ganz, 2004; Ross, 1999).
Pathogenesis of normal tissue side effects
Michael C. Joiner, Albert J. van der Kogel in Basic Clinical Radiobiology, 2018
Telangiectasia, i.e. pathologically dilated capillaries, is observed in virtually all irradiated tissues and organs. The pathogenesis is unclear, but it is assumed that endothelial cell damage is involved. The loss of smooth muscle cells surrounding larger capillaries and veins may also contribute to the development of telangiectasia. In the intestine, the urinary system or also the central nervous system, telangiectasia can be clinically relevant because of the tendency for capillary haemorrhage. In the skin, telangiectasia are mainly a cosmetic problem; they also served, however, as a well-defined quantitative endpoint for radiobiological studies (see Section 14.5). Over longer time periods, the dilated, telangiectatic capillaries may collapse, thus resulting in a reversibility of their consequences, which has been demonstrated, e.g. after radiotherapy for uterine cervix or prostate cancer (15,16).
2,4,6-Trihydroxy-3-geranyl acetophenone suppresses vascular leakage and leukocyte infiltration in lipopolysaccharide-induced endotoxemic mice
Published in Pharmaceutical Biology, 2021
Yee Han Chan, Nazmi Firdaus Musa, Yi Joong Chong, Siti Arfah Saat, Faizul Hafiz, Khozirah Shaari, Daud Ahmad Israf, Chau Ling Tham
The endothelium is a monolayer of endothelial cells lining the inner vascular wall of blood vessels and the lymphatic system, so it is in direct contact with the blood or lymph, and circulating cells. Under normal physiological conditions, the endothelium works as a functional barrier that maintains homeostasis at an optimum level, including the regulation of inflammation, blood fluidity, platelet aggregation, coagulation and vascular tone (Daiber et al. 2017). Of these functions, endothelium’s role in regulating vascular inflammation has been the most extensively studied, as hyperinflammatory responses are deleterious to the hosts since it ultimately induces sepsis and tissue damage (Nedeva et al. 2019). LPS, a component found in the outer membrane of Gram-negative bacteria, is seen as a reason for the problem, as it can trigger the exacerbation of vascular inflammation and thus lead to the activation of endothelial cells through compromised adhesive properties and increased endothelial permeability (Li et al. 2016). Upon activation, the overproduction of proinflammatory mediators, such as leukotrienes, prostaglandins, cytokines and chemokines, leads to endothelial hyperpermeability; and thus, resulting in the unrestricted passage of plasma proteins (Abdulkhaleq et al. 2018). These events cause excessive fluid leakage that ultimately leads to endotoxemia and septic shock (Kottke and Walters 2016).
Endothelial function in patients with atrial fibrillation
Published in Annals of Medicine, 2020
Ahsan A. Khan, Graham N. Thomas, Gregory Y. H. Lip, Alena Shantsila
Endothelium refers to cells that line the interior surface of blood vessels, forming an interface between circulating blood in the lumen and the vessel wall. It is a single layer of simple squamous cells lining the entire circulatory system, from the heart to the smallest capillaries [7]. Endothelium is mesodermal in origin. In a straight section of a blood vessel, vascular endothelial cells typically align and extend in the direction of fluid flow. Endothelial cells are able to alter their structure and phenotype depending on the vessel type. For example, endothelial cells lining the artery tend to be thicker than those in capillaries, which are fenestrated and thinner to allow for exchange of gases, nutrients and metabolites. Furthermore, endothelial cells can respond differently to stimulation in different vascular beds and even in different sections of the same vascular bed [8–10].
The protective effect of tanshinone IIa on endothelial cells: a generalist among clinical therapeutics
Published in Expert Review of Clinical Pharmacology, 2021
Jun Feng, Lina Liu, Fangfang Yao, Daixing Zhou, Yang He, Junshuai Wang
The endothelium is a single layer of cells that overlays the lumen of blood vessels and plays an important physiological role in vascular homeostasis. The endothelial cells integrate and modulate the fundamental functions of the vascular wall, which controls inflammation, coagulation, and thrombosis, as well as regulates vasomotion. Many of these functions are mediated through the release of nitric oxide (NO). Endothelial injury involves a complex pathophysiological process that includes both increased activation of endothelial cells and the initiation of endothelial dysfunction, leading to vascular damage in both metabolic and atherosclerotic diseases, including cardiovascular diseases, neurodegenerative disorders, pulmonary diseases, hypertension, renal diseases, cancer, and metabolic diseases (such as hyperglycemia or diabetes and hyperlipidemia) [10–12]. Taken together, endothelial cells mediate important physiological functions, including the maintenance of blood fluidity, modulation of vascular tone, regulation of inflammation and immune response, and management of oxidative stress and neovascularization.