Download Gastrointestinal Mucosal Repair and Experimental by C.-H. Cho, J.-Y. Wang, C. Sakamoto PDF
By C.-H. Cho, J.-Y. Wang, C. Sakamoto
Over the past decade, massive growth has been made in knowing mobile and molecular mechanisms curious about gastrointestinal mucosal damage and service. those findings give you the foundation to spot the etiology and pathogenesis of assorted intestine mucosal injury-related ailments and to advance new healing ways. The booklet to hand is split into 3 sections: Epithelial restitution, mucosal fix and ulcer therapeutic, and experimental therapeutics. the 1st half highlights the early quick mucosal restitution, focussing at the roles of extracellular matrix, cytoskeleton, cytokines, Ca2+ signaling, polyamines, and the protein kinase C / DAG pathways. the following part bargains with points of continual mucosal therapeutic, focusing on the jobs of basic reaction gene expression, angiogenesis and angiogenic development elements, platelets, and the mechanisms of mobile renewal after damage in designated situations. The final half explores new healing ways.
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Additional resources for Gastrointestinal Mucosal Repair and Experimental Therapeutics (Frontiers of Gastrointestinal Research)
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Front Gastrointest Res. Basel, Karger, 2002, vol 25, pp 29–42 Ca2؉ Signaling in Epithelial Restitution Jaladanki N. , USA Calcium ion (Ca2ϩ) is a life and death signal in eukaryotic cells and performs an especially large number of cellular functions. Ca2ϩ acts as an intracellular messenger, relaying information within the cells to coordinate the Ca2ϩ-dependent processes including cell motility, proliferation, differentiation and apoptosis [1–6]. To do all of these cellular functions, Ca2ϩ signals need to be flexible yet precisely regulated.
Tansey MG, Word RA, Hidaka H, Singer HA, Schworer CM, Kamm KE, Stull JT: Phosphorylation of myosin light chain kinase by the multifunctional calmodulin-dependent protein kinase II in smooth muscle cells. J Biol Chem 1992;267:12511–12516. Wang JY, Wang J, Golovina VA, Li L, Platoshyn O, Yuan JX: Role of Kϩ channel expression in polyamine-dependent intestinal epithelial cell migration. Am J Physiol 2000;278:C303–C314. Rao JN, Li L, Golovina VA, Platoshyn O, Strauch ED, Yuan JX, Wang JY: Ca2ϩ-RhoA signaling pathway required for polyamine-dependent intestinal epithelial cell migration.
21] demonstrated that in the IEC-6 and Caco2 cell lines the accelerating effects of EGF, HGF and TGF- on epithelial cell restitution are, in part, mediated by the production of prostaglandins. Their wounding model demonstrated that the enhancing effects on resealing speed were reduced by roughly 50–60% in the presence of piroxicam, which inhibits prostaglandin synthesis. In the IEC-6 cell line, lysophosphatidic acid (LPA), a naturally occurring phospholipid that is released by growth factor-stimulated fibroblasts, also enhances cell migration and inhibits cell proliferation through a TGF- independent pathway [24].