p53 Controls Radiation-Induced Gastrointestinal Syndrome in Mice Independent of Apoptosis
Kirsch, David G.
Santiago, Philip M.
Di Tomaso, Emmanuelle
Sullivan, Julie M.
Jeffords, Laura B.
Korsmeyer, Stanley J.
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CitationKirsch DG, Santiago PM, di Tomaso E, Sullivan JM, Hou WS, Dayton T, Jeffords LB, Sodha P, Mercer KL, Cohen R, Takeuchi O, Korsmeyer SJ, Bronson RT, Kim CF, Haigis KM, Jain RK, Jacks T. p53 controls radiation-induced gastrointestinal syndrome in mice independent of apoptosis. Science. 2010 Jan 29; 327(5965):593-6.
AbstractAcute exposure to ionizing radiation can cause lethal damage to the gastrointestinal (GI) tract, a condition called the GI syndrome. Whether the target cells mediating the GI syndrome are derived from the epithelium or endothelium, and whether the target cells die by apoptosis or other mechanisms, are controversial issues. Studying mouse models, we found that selective deletion of the pro-apoptotic genes Bak1 and Bax from the GI epithelium or from endothelial cells did not protect mice from developing the GI syndrome after subtotal body gamma irradiation. In contrast, selective deletion of p53 from the GI epithelium, but not endothelial cells, sensitized irradiated mice to the GI syndrome. Transgenic mice overexpressing p53 in all tissues were protected from the GI syndrome after irradiation. These results suggest that the GI syndrome is caused by death of GI epithelial cells by a mechanism that is regulated by p53 but independent of apoptosis.
Citable link to this pagehttps://nrs.harvard.edu/URN-3:HUL.INSTREPOS:37366553
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