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Modification of the cellular radiation survival and proliferation response by cell-matrix interactions: implications for integrin targeting in therapeutic approaches for radiation accident patients

Bundeswehr Institute of Radiobiology, Neuherbergstrasse 11, 80937 Munich, Germany

Correspondence: Dr Nils Cordes, MD, Bundeswehr Institute of Radiobiology, Neuherbergstrasse 11, 80937 Munich, Germany. E-mail: cordes@radiation-biology.de

The pathophysiological mechanisms that lead to tissue destruction after exposure to ionising radiation are not fully understood. Recent observations showed that cell adhesion-mediating integrins and their signalling cascades affect cellular behaviour after genotoxic stress. Integrins play an important role in cell-matrix and cell-cell interactions and have been shown to be differentially expressed in irradiated tissue. As part of the immune response following irradiation, integrins may serve as critical membrane receptors on diverse normal cells such as leukocytes, platelets or fibroblasts. Modification of integrin function might influence multi-organ involvement and multi-organ failure, two life-threatening events that occur after irradiation. Both of these diseases are predominantly triggered by the immune system, and inhibition of integrin-mediated leukocyte stimulation could support the prevention of severe autoaggressive destruction of tissue. Here we review the evidence that cell-matrix interactions via focal adhesion-associated proteins and integrins, including their signal transduction pathways, play a crucial role in the cellular radiation response and the individual cell's fate after irradiation. In addition, the possible impact of clinically available anti-integrin treatment strategies for radiation accident patients is discussed.