| Item type |
文献 / Documents(1) |
| 公開日 |
2018-05-28 |
| アクセス権 |
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|
アクセス権 |
open access |
| 資源タイプ |
|
|
資源タイプ識別子 |
http://purl.org/coar/resource_type/c_6501 |
|
資源タイプ |
journal article |
| 出版社版DOI |
|
|
|
識別子タイプ |
DOI |
|
|
関連識別子 |
https://doi.org/10.2152/jmi.54.19 |
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|
言語 |
ja |
|
|
関連名称 |
10.2152/jmi.54.19 |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| タイトル |
|
|
タイトル |
Angiotensin II inhibits insulin-induced actin stress fiber formation and glucose uptake via ERK1/2 |
|
言語 |
en |
| 著者 |
Nazari, Hossein
髙橋, 章
原田, 永勝
馬渡, 一諭
ナカノ, マサユキ
岸, 和弘
蛯名, 洋介
中屋, 豊
|
| 抄録 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
There is crosstalk in intracellular signaling between Angiotensin II (Ang II) and insulin. We hypothesized that the underlying mechanism might be related to changes in cytoskeleton. In the presence of 100 nM of Ang II, insulin-induced glucose uptake was decreased and insulin-induced actin filament organization was inhibited. PKC inhibitors, including GF 109203x and p38 MAPK inhibitor (SB 203580) neither improved insulin-induced actin reorganization nor glucose uptake. In contrast, the Ang II-induced inhibition of glucose uptake and actin filament disorganization was reversed by 10 μmol ERK 1/2 MAPK inhibitor (PD 98059). Pretreatment of Ang II increased ERK1/2 phosphorylation and inhibited insulin-induced Akt phosphorylation. The effect of Ang II on ERK 1/2 phosphorylation was blocked by Ang II type 1 receptor antagonists, RNH 6270 and PD 98059 but not by SB 203580 or Guanosine-5’-O-(2-ThioDiphosphate), a G-protein inhibitor. We next tested the effect of broad-spectrum matrix metalloproteinase (MMP) inhibitor (GM 6001) on Ang II-inhibition of insulin signaling pathway. GM 6001 did not improve Ang II-induced actin filament disorganization and did not inhibit ERK1/2 phosphorylation. From these data in L6 myotube, we conclude that Ang II negatively regulates the insulin signal not through MMP signaling pathway but specifically through MMP-independent ERK 1/2 activation pathway, providing an alternative molecular mechanism for angiotensin-induced insulin resistance. |
|
言語 |
en |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
insulin |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
angiotensin II |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
cytoskeleton |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
angiotensin receptor blockers |
| キーワード |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
matrix metalloproteinase |
| 書誌情報 |
en : The Journal of Medical Investigation
巻 54,
号 1-2,
p. 19-27,
発行日 2007-02
|
| 収録物ID |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
13496867 |
| 収録物ID |
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|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
13431420 |
| 収録物ID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA11166929 |
| 収録物ID |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AA12022913 |
| 出版者 |
|
|
出版者 |
Faculty of Medicine Tokushima University |
|
言語 |
en |
| EID |
|
|
識別子 |
148371 |
|
識別子タイプ |
URI |
| 言語 |
|
|
言語 |
eng |
jmi_54_1-2_19.pdf (1010 KB)
