| Item type |
学術雑誌論文 / Journal Article(1) |
| 公開日 |
2011-06-23 |
| タイトル |
|
|
タイトル |
MCP-1 INHIBITS DNA SYNTHESIS IN RAT PANCREATIC STELLATE CELLS |
|
言語 |
en |
| 言語 |
|
|
言語 |
eng |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
MCP-1 |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
CCR2 |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Pancreatic stellate cells |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
DNA replication |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Autocrine |
| 主題 |
|
|
言語 |
en |
|
主題Scheme |
Other |
|
主題 |
Paracrine |
| 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 |
| アクセス権 |
|
|
アクセス権 |
open access |
|
アクセス権URI |
http://purl.org/coar/access_right/c_abf2 |
| 作成者 |
KAMADA, Kentaro
MASHIMA, Hirosato
GOTO, Takashi
OHNISHI, Hirohide
|
| 内容記述 |
|
|
内容記述タイプ |
Abstract |
|
内容記述 |
Activated pancreatic stellate cells (PSCs) synthesize various kinds of cytokines and chemokines including monocyte chemoattractant protein-1 (MCP-1) and play major roles in promoting inflammation and fibrogenesis in the pancreas. MCP-1 is a potent chemotactic factor for leukocytes and it has recently been shown that the target is not restricted. The aim of this study was to investigate whether MCP-1 exerts a biological effect on PSCs. Cultured rat PSCs secreted MCP1 independent of the concentration of transforming growth factor-β1 (TGF-β 1) in the culture media. Although PSCs lack the typical receptor system (C-C chemokine receptor 2 (CCR2)), MCP-1 inhibited DNA synthesis in PSCs without activation, suggesting the presence of CCR2-independent MCP-1 signaling pathway. Further, MCP-1 inhibited the proliferation of PSCs in which TGF-β 1/Smad pathway was blocked by the dominant-negative Smad2/3 over-expression. MCP-1 did not affect the phosphorylation state of mitogen-activated protein kinase (MAPK), Akt, nor epidermal growth factor receptor (EGFR). Taken together, MCP-1 inhibited DNA synthesis of cultured rat PSCs in an autocrine or paracrine manner without activation and this effect was exerted through CCR2-independent and TGF-β1/Smad-independent pathway. These data provide new insights to better understand MCP-1 participation in pancreatic inflammation and also to develop a new strategy for its treatment. |
|
言語 |
en |
| 出版タイプ |
|
|
出版タイプ |
VoR |
|
出版タイプResource |
http://purl.org/coar/version/c_970fb48d4fbd8a85 |
| 書誌情報 |
ja : 秋田医学
巻 36,
号 3-4,
p. 185-194,
発行日 2010-03-01
|
| 収録物識別子 |
|
|
収録物識別子タイプ |
ISSN |
|
収録物識別子 |
03866106 |
| 収録物識別子 |
|
|
収録物識別子タイプ |
NCID |
|
収録物識別子 |
AN00009294 |
| 出版者 |
|
|
出版者 |
秋田医学会 |
|
言語 |
ja |
akitai36(185).pdf (504.5 kB)
