In:
Human & Experimental Toxicology, SAGE Publications, Vol. 30, No. 8 ( 2011-08), p. 876-883
Abstract:
Radiation-induced pneumonitis is closely associated with the interplay of various stress-activated signals and immune responses related to the progression of lung injury. Mitogen-activated protein (MAP) kinase pathways play critical roles in the progression of inflammation via a cellular damage. Here, we examined the regional distribution of phosphorylated MAP kinases (p-JNK, p-ERK, and p-p38) in the progression of pneumonitis after exposure of a single dose irradiation with 10 Gy for 0, 4, and 8 weeks in rats. Also, we identified positive cells for these kinases using specific cell-type markers related to inflammation and type II pneumocyte. p-JNK was present abundantly in activated macrophages, CD8 + T-cells, peribronchiolar smooth muscle cells, and weakly type II pneumocytes at 4 weeks or 8 weeks after irradiation. p-p38 and p-ERK was predominantly expressed in macrophages, CD4 + T-cells, fibrotic cells as well as present in various lung parenchymal cells including alveolar epithelial cells and type II pneumocytes. In conclusion, it is considered that MAP kinase pathways play a pivotal role in early damage of residual cells as well as in the long-term regulation of distinct inflammatory cells during the progression of radiation-induced pneumonitis.
Type of Medium:
Online Resource
ISSN:
0960-3271
,
1477-0903
DOI:
10.1177/0960327110382562
Language:
English
Publisher:
SAGE Publications
Publication Date:
2011
detail.hit.zdb_id:
1483723-7
