Gastrointestinal Mucosal Repair and Experimental - download pdf or read online

By C.-H. Cho, J.-Y. Wang, C. Sakamoto

ISBN-10: 3805573820

ISBN-13: 9783805573825

During the last decade, substantial development has been made in figuring out mobile and molecular mechanisms focused on gastrointestinal mucosal damage and service. those findings give you the foundation to spot the etiology and pathogenesis of assorted intestine mucosal injury-related illnesses and to strengthen new healing methods. The ebook 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 elements of power mucosal therapeutic, targeting the jobs of basic reaction gene expression, angiogenesis and angiogenic progress components, platelets, and the mechanisms of mobile renewal after damage in exact situations. The final half explores new healing methods.

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Extra info for Gastrointestinal Mucosal Repair and Experimental Therapeutics (Frontiers of Gastrointestinal Research)

Example text

13] showed that EGF has important regulatory effects on actin filaments leading to increased stress Yoo/Lotz/Matthews 22 fiber formation. The resultant cytoskeletal rearrangements are necessary for the initiation of motility in IEC-6 cells. Alterations in actin fibers lead to cell flattening and the formation of lamellipodia and membrane ruffling, which are early phenotypic changes of migratory cells. Santos found that this effect of EGF is mediated through Rho GTPases, and that specific inhibition of Rho proteins inhibited motility following wounding [13].

Cells surrounding the damage flatten and those immediately adjacent to the wound extend lamellipodia, broad, thin cytoplasmic protrusions, to cover the mucosal defect [26]. Lamellipodia appear to generate the force required to induce cell flattening. Actin filaments inside lamellipodia engage integrins, cell surface proteins that adhere to underlying matrix proteins. Adhesive strength between integrins and the stationary matrix generates the traction, transmitted to the cell cytoplasm via actin filaments, to stretch the epithelial cells over the matrix.

R. , USA Gastrointestinal epithelial damage can result from infection (ulcer), chemical agents (alcohol, drugs), or mechanical forces (stretching) and requires prompt repair to preserve the epithelial barrier to luminal antigens. Although repair is a continuous process, it can be divided into two stages depending on whether the primary action is one of cell spreading and migration or of proliferation. During the early restitution period (conservatively up to 12 h), viable cells bordering the lesion extend lamellipodia and migrate over the damaged area.

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Gastrointestinal Mucosal Repair and Experimental Therapeutics (Frontiers of Gastrointestinal Research) by C.-H. Cho, J.-Y. Wang, C. Sakamoto


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