著者 佐藤 千景|
発行日 2011-12-01
出版物タイトル 岡山医学会雑誌
123巻
3号
資料タイプ 学術雑誌論文
JaLCDOI 10.18926/AMO/46850
フルテキストURL 65_4_247.pdf
著者 Watanabe, Naomi| Shikata, Kenichi| Shikata, Yasushi| Sarai, Kei| Omori, Kazuyoshi| Kodera, Ryo| Sato, Chikage| Wada, Jun| Makino, Hirofumi|
抄録 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.
キーワード diabetic nephropathy ICAM-1 ERK p38 MAPK JNK
Amo Type Original Article
発行日 2011-08
出版物タイトル Acta Medica Okayama
65巻
4号
出版者 Okayama University Medical School
開始ページ 247
終了ページ 257
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 21860531
Web of Sience KeyUT 000294236700005
JaLCDOI 10.18926/AMO/45266
フルテキストURL 65_2_81.pdf
著者 Sasaki, Motofumi| Shikata, Kenichi| Okada, Shinichi| Miyamoto, Satoshi| Nishishita, Shingo| Usui Kataoka, Hitomi| Sato, Chikage| Wada, Jun| Ogawa, Daisuke| Makino, Hirofumi|
抄録 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.
キーワード kidney inflammation chemokine
Amo Type Original Article
発行日 2011-04
出版物タイトル Acta Medica Okayama
65巻
2号
出版者 Okayama University Medical School
開始ページ 81
終了ページ 89
ISSN 0386-300X
NCID AA00508441
資料タイプ 学術雑誌論文
言語 English
著作権者 CopyrightⒸ 2011 by Okayama University Medical School
論文のバージョン publisher
査読 有り
PubMed ID 21519365
Web of Sience KeyUT 000289818800003