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ID 46850
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Thumnail 65_4_247.pdf 7.75 MB
Author
Watanabe, Naomi
Shikata, Kenichi Kaken ID researchmap
Shikata, Yasushi
Sarai, Kei
Omori, Kazuyoshi
Kodera, Ryo
Makino, Hirofumi
Abstract
Inflammatory processes are involved in the pathogenesis of diabetic nephropathy. The aim of this study was to clarify the role of mitogen-activated protein kinase (MAPK) pathways for induction of intercellular adhesion molecule-1 (ICAM-1) expression in glomerular endothelial cells under diabetic conditions. We examined the expression of ICAM-1 in the kidneys of experimental diabetic rats. Human glomerular endothelial cells (GE cells) were exposed to normal glucose concentration, high glucose concentration (HG), or high mannitol concentration (HM), and then the expression of the ICAM-1 protein and the phosphorylation of the 3 subfamilies of mitogen-activated protein kinase (MAPK) were determined using Western blot analysis. Next, to evaluate the involvement of MAPKs in HG- or HM-induced ICAM-1 expression, we preincubated GE cells with the inhibitors for ERK, p38 or JNK 1h prior to the application of glucose or mannitol. Expression of ICAM-1 was increased in the glomeruli of diabetic rats. Both HG and HM induced ICAM-1 expression and phosphorylation of ERK1/2, p38 and JNK in GE cells. Expression of ICAM-1 was significantly attenuated by inhibitors of ERK, p38 and JNK. We conclude that activation of ERK1/2, p38 and JNK cascades may be involved in ICAM-1 expression in glomerular endothelial cells under diabetic conditions.
Keywords
diabetic nephropathy
ICAM-1
ERK
p38 MAPK
JNK
Amo Type
Original Article
Published Date
2011-08
Publication Title
Acta Medica Okayama
Volume
volume65
Issue
issue4
Publisher
Okayama University Medical School
Start Page
247
End Page
257
ISSN
0386-300X
NCID
AA00508441
Content Type
Journal Article
language
英語
Copyright Holders
CopyrightⒸ 2011 by Okayama University Medical School
File Version
publisher
Refereed
True
PubMed ID
Web of Science KeyUT