Regulation intercellular

The n-3 PUFAs are reported to reduce expression of endothelial adhesion molecules VCAM-1, E-selectin, and ICAM-1, therefore influencing leukocyte-endothelial cell interactions and leukocyte migration across the endothelium. 105,106 Oxidized EPA has been shown to be a more potent inhibitor of leukocyte-endothelial interaction, in vitro and in vivo, than EPA.107 Since EFAs regulate intercellular adhesion, it has been speculated that the skin changes that are observed in EFA deficiency, may be due, at least in part, to damaged cell adhesion.108 n-3 PUFAs and GLA supplementation enhance E-cadherin expression in cancer cells and this possibly reduces the invasiveness of these cells.109... 

Ayars, G.H., Altman, L.C, Loegering, D.A. and Gleich, G.J. (1991). Eosinophil major basic protein [MBP] up regulates intercellular adhesion molecular-1 [ICAM-1] expression on human nasal epithelial cells [HNE]. J. Allergy Clin. Inununol. 87, 304. 

Gap junction channels provide pathways for direct current flow between cells and for regulated intercellular movement of important cellular signaling molecules, including cyclic nucleotides (5, 13-17). Consequently, gap junction channels are thought to play crucial regulatory roles in cell biology, development,and physiology (18-22). 

TNF also up-regulates intercellular adhesion molecule 1 (ICAM-1) on glial cells and leukocyte functional antigen (LFA)-1)32, but not LFA-la,... 

Schofield L, Novakovic S, Gerold P, Schwarz RT, McConville MJ, Tachado SD 1996. Gly-cosylphosphatidylinositol toxin of Plasmodium up-regulates intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and E-selectin expression in vascular endothelial cells and increases leukocyte and parasite cytoadherence via tyrosine kinase-dependent signal transduction. J Immunol 156 1886-1896. 

Although gap junctions allow cells to communicate metabolically under normal conditions, the ability to close gap junctions provides the tissue with an important intercellular regulation mechanism. In addition, gap junctions provide a means to protect adjacent cells if one or more cells are damaged or... 

Allostery is the key chemical process that makes possible intracellular and intercellular regulation . . the molecular interac-... 

The regulation of the total peripheral resistance also involves the complex interactions of several mechanisms. These include baroreflexes and sympathetic nervous system activity response to neurohumoral substances and endothelial factors myogenic adjustments at the cellular level, some mediated by ion channels and events at the cellular membrane and intercellular events mediated by receptors and mechanisms for signal transduction. As examples of some of these mechanisms, there are two major neural reflex arcs (Fig. 1). Baroreflexes are derived from high-pressure barorecep-tors in the aortic arch and carotid sinus and low-pressure cardiopulmonary baroreceptors in ventricles and atria. These receptors respond to stretch (high pressure) or... 

TRPVl also plays a central role in intercellular pro-inflammatory feedback loops. An important example is mast cells and sensory nerves. Mast cells release tryptase that, in turn, activates the protease-activated receptor PAR-2 activation of PAR-2 then opens TRPVl via PKC [50]. In keeping with this, PAR-2 agonists reduce the heat activation threshold of TRPVl from 42 °C to below body temperature [51]. Excited nerve endings release SP that, as a positive feedback, binds to neurokinin NKl receptors on mast cells. Mast cells also express TRPVl [52]. Consequently, endovanilloids can act in concert to stimulate mast cells and activate capsaicin-sensitive nerve endings. Of relevance is the finding that PAR-2 is up-regulated in the bladder during experimental cystitis [53]. 

Intercellular communication can be affected by different carotenoids and their oxidation products, and opposing effects can be observed depending on their concentrations (Stahl et al., 1998). Carotenoids play a role in the induction and stimulation of intercellular communication via gap junctions, which in turn play an important role in the regulation of cell growth, differentiation, and apoptosis (Tapiero et al., 2004). 

Haraldsen, G., Kvale, D., Lien, B., Farstad, I.N. and Brandtzaeg, P. (1996) Cytokine-regulated expression of E-selectin, intercellular adhesion molecule-1 (IGAM-1), and vascular cell adhesion molecule-1 (VGAM-1) in human microvascular endothelial cells. Journal of Immunology 156, 2558-2565. 

Alveolar epithelial cells (AECs) are connected with each other by various epithelial cell-cell contacts (i.e., tight junctions, adherens junctions and others). These contacts comprise several groups of proteins, such as occludin, zonula occludens (ZO-1, -2, -3), claudins, tricellulin, E-cadherin and intercellular adhesion molecule-1 (ICAM-1) [13-15], Their regulation and interplay, which has influence on epithelial barrier properties, however, is largely unknown to date. 

One of the main functions of epithelia is to control water and solutes, compartmentalized by the regulation of transport across the epithelium from body interior to exterior (or vice versa). Deviations from the meticulously regulated movement of water and solutes across the epithelial barrier can lead to states of disease and can be detrimental to life. Fluids can traverse epithelia by one of two routes through the cells (transcellular transport) or between cells (intercellular or paracellular transport) (Figure 15.1A). 

The theoretical model that best describes regulation of transepithelial transport is derived from the Ussing-Zerahn equivalent electrical circuit model of ion transport theory [57] (Figure 15.1B). The model predicts that epithelia are organized as a layer(s) of confluent cells, where plasma membranes of neighboring cells come into close contact and functionally occlude the intercellular space. Accordingly, molecules can move across epithelia either through the cells... 

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