Endothelial cells, protein-mediated cell

Endothelial cells, protein-mediated cell adhesion on biomaterials, 143... 

Boulday G, Haskova Z, Reinders ME, Pal S, Briscoe DM. Vascular endothelial growth factor-induced signaling pathways in endothelial cells that mediate overexpression of the chemokine IFN-(gamma)-inducible protein of lOkDa in vitro and in vivo. J Immunol 2006 176(5) 3098-3107. 

Fig. 8. Schematic representation of protein-mediated cell adhesion on biomaterial surfaces. Biomaterial surface properties (such as hydrophilicity/hydrophobicity, topography, energy, and charge) affect subsequent interactions of adsorbed proteins these interactions include but are not limited to adsorbed protein type, concentration, and conformation. Changes in protein-surface interactions may alter accessibility of adhesive domains (such as the peptide sequence arginine-glycine-aspartic acid) to cells (such as osteoblasts, fibroblasts, or endothelial cells) and thus modulate cellular adhesion. (Adapted and redrawn from Schakenraad, 1996.)...

Akarasereenont, P.C., Techatraisak, K., Thaworn, A., and Chotewuttakorn, S. (2002) The Expression of COX-2 in VEGF-Treated Endothelial Cells Is Mediated Through Protein Tyrosine Kinase, Medial. Inflamm. 11,17 22. 

Shen XY. Hamilton TA, DiCorleto PE Lipopolysaccharide-induced expression of the competence gene KC m vascular endothelial cells is mediated through protein kinase C J Cell Physiol 1989, 140 44-51... 

AMPK can also be activated by a Ca2+-mediated pathway involving phosphorylation at Thr-172 by the Ca2+/calmodulin-dependent protein kinase, CaMKK 3. CaMKKa and CaMKK 3 were discovered as the upstream kinase for the calmodulin-dependent protein kinases-1 and -IV they both activate AMPK in a Ca2+/ calmodulin-dependent manner in cell-free assays, although CaMKK 3 appears to much more active against AMPK in intact cells. Expression of CaMKKa and CaMKK(3 primarily occurs in neural tissues, but CaMKKp is also expressed in some other cell types. Thus, the Ca2+-mediated pathway for AMPK activation has now been shown to occur in response to depolarization in rat neuronal tissue, in response to thrombin (acting via a Gq-coupled receptor) in endothelial cells, and in response to activation of the T cell receptor in T cells. 

Many low weight compounds produced by microor-ganism-like formylated peptides as well as endogenous mediators are chemotactic for leukocytes and promote the inflammatory process. The main endogenous compounds are listed in Table 1 and are derived from activated plasma protein cascades that function as amplification mechanisms, are performed and released from activated cells or are de novo synthesized on demand by cells participating in or being affected by inflammatory events. The major modulators of leukocyte adhesion to endothelial cells are listed in Table 2. 

Figure 2. (1) Neutrophils circulating passively in blood capillary. (2) Chemoattractants may be detected by the circulating neutrophils, by the endothelial cells lining the lumen, or both in order that the neutrophils become adhesive. This adhesion is mediated by selectins, a group of cell surface proteins. Neutrophils roll on the surface of the endothelial cells and then actively locomote seeking out spaces between the endothelial cells. (3) The adhesive neutrophils begin to squeeze between endothelial cells. (4) Cells move through the extracellular matrix towards the site of infection. Here adhesion is low and may not be necessary for locomotion. (5) At the site of infection, neutrophils become trapped by increased adhesion where they phagocytose bacteria and liberate the contents of their granules. After Lackie (1982,1986).

There may be substantial variation both within and among species (e.g., in mice vs. humans) in the expression of various proteins, receptors and/or ligands that influence the activation of mast cells (or basophils or other potential effector cell types), or that can regulate the responsiveness of end organ target cells (e.g., bronchial or gastrointestinal smooth muscle cells, vascular endothelial cells) to potential mediators of anaphylaxis derived from mast cells. 

Nakamuta S, Endo H, Higashi Y, Kousaka A, Yamada H, Yano M, Kido H (2008) Human immunodeficiency virus type 1 gpl20-mediated disruption of tight junction proteins by induction of proteasome-mediated degradation of zonula occludens-1 and -2 in human brain microvascular endothelial cells. J Neurovirol 14 186-195... 

---