ID 110870
Author
Soda, Akira Department of Physiology, Pathophysiological Preventive Medicine, Institute of Health Biosciences, the University of Tokushima Graduate School
Ikehara, Toshitaka Department of Physiology, Pathophysiological Preventive Medicine, Institute of Health Biosciences, the University of Tokushima Graduate School
Kinouchi, Yohsuke Life System, Institute of Technology and Science, Graduate School, the University of Tokushima Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Yoshizaki, Kazuo Department of Physiology, Pathophysiological Preventive Medicine, Institute of Health Biosciences, the University of Tokushima Graduate School Tokushima University Educator and Researcher Directory KAKEN Search Researchers
Keywords
ELF-EMF
ERK1/2
PI3K
p38 MAPK
collagen
osteoblast
MC3T3-E1 cell
Content Type
Journal Article
Description
The effect of exposure to extremely low frequency-electromagnetic field (ELFEMF : 3 mT, 60 Hz) on differentiation of mouse osteoblast-like MC3T3-E1 cells was examined together with addition of insulin-like growth factor I (IGF-I). As a marker of the differentiation, the cellular collagen content was determined by the absorbance of Sirius red-stained cells measured at the wavelength of 510-520 nm with an imaging microspectroscopy. Exposure to ELF-EMF increased significantly the collagen in the cells. Treatment with PD98059, an inhibitor of extracellular signal-regulated kinase 1/2 (ERK1/2) activation, reduced the collagen in all of the cells examined on control, IGF-I addition and ELFEMF exposure, however, PD98059 did not prevent the increase in the collagen caused by ELF-EMF exposure, and IGF-I also increased the collagen in the presence of the inhibitor. When phosphatidylinositol 3-kinase (PI3K) pathway was inhibited by LY294002, the increase in collagen induced by ELF-EMF exposure was accelerated, however, the increase in collagen observed by IGF-I addition was suppressed. Treatment with SB203580, an inhibitor of p38 mitogen-activated protein kinase (p38 MAPK), suppressed the increase in the collagen induced by ELF-EMF exposure, whereas IGF-I addition increased the collagen in the presence of the inhibitor. These results suggested that collagen synthesis stimulated by ELF-EMF exposure was carried out by the participation of p38 MAPK pathway, and that PI3K pathway may have the role to suppress the collagen synthesis induced by ELF-EMF exposure, and that the suppression of the PI3K pathway may allow the acceleration of the collagen synthesis.
Journal Title
The journal of medical investigation : JMI
ISSN
13431420
NCID
AA11166929
Volume
55
Issue
3-4
Start Page
267
End Page
278
Sort Key
267
Published Date
2008-08
EDB ID
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher
departments
Science and Technology
Medical Sciences