Mice Lacking RIP3 Kinase are not Protected from Acute Radiation Syndrome.

Published

Journal Article

Exposure to high doses of ionizing radiation can cause lethal injury to normal tissue, thus inducing acute radiation syndrome. Acute radiation syndrome is caused by depletion of bone marrow cells (hematopoietic syndrome) and irreparable damage to the epithelial cells in the gastrointestinal tract (gastrointestinal syndrome). Although radiation initiates apoptosis in the hematopoietic and gastrointestinal compartments within the first few hours after exposure, alternative mechanisms of cell death may contribute to injury in these radiosensitive tissues. In this study, we utilized mice lacking a critical regulator of necroptosis, receptor interacting protein 3 (RIP3) kinase, to characterize the role of RIP3 in normal tissue toxicity after irradiation. Our results suggest that RIP3-mediated signaling is not a critical driver of acute radiation syndrome.

Full Text

Duke Authors

Cited Authors

  • Castle, KD; Daniel, AR; Moding, EJ; Luo, L; Lee, C-L; Kirsch, DG

Published Date

  • June 2018

Published In

Volume / Issue

  • 189 / 6

Start / End Page

  • 627 - 633

PubMed ID

  • 29634408

Pubmed Central ID

  • 29634408

Electronic International Standard Serial Number (EISSN)

  • 1938-5404

Digital Object Identifier (DOI)

  • 10.1667/RR15001.1

Language

  • eng

Conference Location

  • United States