Author Sato, Chikage|
Published Date 2011-12-01
Publication Title 岡山医学会雑誌
Volume volume123
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/46850
FullText URL 65_4_247.pdf
Author Watanabe, Naomi| Shikata, Kenichi| Shikata, Yasushi| Sarai, Kei| Omori, Kazuyoshi| Kodera, Ryo| Sato, Chikage| Wada, Jun| 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 21860531
Web of Science KeyUT 000294236700005
JaLCDOI 10.18926/AMO/45266
FullText URL 65_2_81.pdf
Author Sasaki, Motofumi| Shikata, Kenichi| Okada, Shinichi| Miyamoto, Satoshi| Nishishita, Shingo| Usui Kataoka, Hitomi| Sato, Chikage| Wada, Jun| Ogawa, Daisuke| Makino, Hirofumi|
Abstract Glomerular hyperfiltration is a common pathway leading to glomerulosclerosis in various kinds of kidney diseases. The 5/6 renal ablation is an established experimental animal model for glomerular hyperfiltration. On the other hand, low-grade inflammation is also a common mechanism for the progression of kidney diseases including diabetic nephropathy and atherosclerosis. Here we analyzed the gene expression profile in the remnant kidney tissues of 5/6 nephrectomized mice using a DNA microarray system and compared it with that of sham-operated control mice. The 5/6 nephrectomized mice showed glomerular hypertrophy and an increase in the extracellular matrix in the glomeruli. DNA microarray analysis indicated the up-regulated expression of various kinds of genes related to the inflammatory process in remnant kidneys. We confirmed the up-regulated expression of platelet factor-4, and monocyte chemoattractant protein-1, 2, and 5 in remnant kidneys by RT-PCR. The current results suggest that the inflammatory process is involved in the progression of glomerulosclerosis and is a common pathway of the pathogenesis of kidney disease.
Keywords kidney inflammation chemokine
Amo Type Original Article
Published Date 2011-04
Publication Title Acta Medica Okayama
Volume volume65
Issue issue2
Publisher Okayama University Medical School
Start Page 81
End Page 89
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 21519365
Web of Science KeyUT 000289818800003