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21 - Regulation of Cell Death in the Gastrointestinal Tract

from Part II - Cell Death in Tissues and Organs

Published online by Cambridge University Press:  07 September 2011

Douglas R. Green
Affiliation:
St. Jude Children's Research Hospital, Memphis, Tennessee
Maria Eugenia Guicciardi
Affiliation:
Mayo Clinic College of Medicine
Gregory J. Gores
Affiliation:
Mayo Clinic College of Medicine
John C. Reed
Affiliation:
Sanford-Burnham Medical Research Institute, La Jolla, California
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Summary

Introduction

The gastrointestinal (GI) tract begins with the mouth, leads to the esophagus, and extends through the stomach, small intestine (including duodenum, jejunum, and ileum), and large intestine (divided into cecum and colon), to end at the anus. In addition, the GI tract includes three accessory organs: liver, gallbladder, and pancreas. The liver produces bile, a fluid containing molecules (bile acids) that help the digestion of lipids, and, via numerous canaliculi forming the biliary system, secretes it into the gallbladder, where it is stored and concentrated. Upon eating, bile is discharged into the small intestine. The pancreas is a dual-function gland, working as both an endocrine and an exocrine gland. The exocrine pancreas secretes pancreatic juice containing bicarbonate and several enzymes, including trypsin, chymotrypsin, lipase, and pancreatic amylase, into the small intestine. Both the liver and the pancreas aid in the digestive process.

Type
Chapter
Information
Apoptosis
Physiology and Pathology
, pp. 231 - 239
Publisher: Cambridge University Press
Print publication year: 2011

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References

Akazawa, Y., Gores, G.J. Death receptor-mediated liver injury. Semin Liver Dis 2007;27:327–38
Algul, H., Treiber, M., Lesina, M., Nakhai, H., Saur, D., Geisler, F., Pfeifer, A., Paxian, S., Schmid, R.M. Pancreas-specific RelA/p65 truncation increases susceptibility of acini to inflammation-associated cell death following cerulean pancreatitis. J Clin Invest 2007;117:1490–501
Bernstein, C., Bernstein, H., Payne, C.M., Dvorak, K., Garewal, H. Field defects in progression to gastrointestinal tract cancers. Cancer Lett 2008;260:1–10
Edelblum, K.L., Yan, F., Yamaoka, T., Polk, B. Regulation of apoptosis during homeostasis and disease in the intestinal epithelium. Inflamm Bowel Dis 2006;12:413–24
Fabregat, I., Roncero, C., Fernández, M. Survival and apoptosis: a dysregulated balance in liver cancer. Liver Int 2007;27:155–62
Feldstein, A.E., Canbay, A., Guicciardi, M.E., Higuchi, H., Bronk, S.F., Gores, G.J. Diet associated hepatic steatosis sensitizes to Fas mediated liver injury in mice. J Hepatol 2003;39:978–83
Hezel, A.F., Kimmelman, A.C., Stanger, B.Z., Bardeesy, N., DePinho, R.A. Genetics and biology of pancreatic ductal adenocarcinoma. Genes Dev 2006;20:1218–49
Kaser, A., Lee A, H., Franke, A., Glickman, J.N., Zeissig, S., Tilg, H., Nieuwenhuis, E.E.S., Higgins, D.E., Schreiber, S., Glimcher, L.H., Blumberg, R.S. XBP1 links ER stress to intestinal inflammation and confers genetic risk for human inflammatory bowel disease. Cell 2008;134:743–56
Qiu, W., Carson-Walter, E.B., Liu, H., Epperly, M., Greenberger, J.S., Zambetti, G.P., Zhang, L., Yu, J. PUMA regulates intestinal progenitor cell radiosensitivity and gastrointestinal syndrome. Cell Stem Cell 2008;2:576–83
Radtke, F., Clevers, H. Self-renewal and cancer of the gut: two sides of a coin. Science 2005;307:1904–9
Schattenberg, J.M., Galle P, R., Schuchmann, M. Apoptosis in liver disease. Liver Int 2006;26:904–11
Van Der Woude, C.J., Kleibeuker, J.H., Jansen, P.L., Moshage, H. Chronic inflammation, apoptosis and (pre-)malignant lesions in the gastrointestinal tract. Apoptosis 2004;9:123–30
Wroblewski, L.E., Peek, R.M. Jr. Orchestration of dysregulated epithelial turnover by a manipulative pathogen. Cell Host Microbe 2007;2:209–11
Zou, C., Ma, J., Wang, X., Guo, L., Zhu, Z., Stoops, J., Eaker, A.E., Johnson, C.J., Strom, S., Michalopoulos, G.K., DeFrances, M.C., Zarnegar, R. Lack of Fas antagonism by Met in human fatty liver disease. Nat Med 2007;13:1078–85

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