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Effect of nitric oxide donor and gamma irradiation on MAPK signaling in murine peritoneal macrophages
Author(s) -
Narang Himanshi,
Krishna Malini
Publication year - 2008
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.21429
Subject(s) - radioresistance , nitric oxide , mapk/erk pathway , sodium nitroprusside , macrophage , microbiology and biotechnology , protein kinase a , p38 mitogen activated protein kinases , kinase , apoptosis , chemistry , phagocytosis , signal transduction , cancer research , biology , cell culture , biochemistry , in vitro , endocrinology , genetics
Irradiation (IR) of cells is known to activate enzymes of mitogen activated protein kinase (MAPK) family. These are known to be involved in cellular response to stress and are determinants of cell death or survival. When radiotherapy is delivered to malignant cells, macrophages, being radioresistant, survive, get activated, and produce large amounts of nitric oxide. As a result of activation they recognize and phagocytose tumor and normal cell apoptotic bodies leading to tumor regression. In this study, the MAPK signaling in peritoneal macrophages was investigated which plays an important role in its various functions, in an environment which is predominantly nitric oxide, as is after IR. The behavior of macrophages in such an environment was also looked at. The three MAPK (ERK1/2, p38, and JNK) respond differently to Sodium nitroprusside (SNP) alone or IR alone. All the three were activated following IR but only JNK was activated following SNP treatment. Surprisingly, when both the stresses were given simultaneously or one after the other, this differential response was lost and there was a complete inhibition of phosphorylation of all the three MAPKs, irrespective of the order of the two insults (IR and SNP). The noteworthy observation was that despite the complete inhibition of MAPK signaling there was no effect on either the viability or the phagocytic efficiency of peritoneal macrophages. J. Cell. Biochem. 103: 576–587, 2008. © 2007 Wiley‐Liss, Inc.