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Sphingosine-1-phosphate receptor type 2 (S1P2) inhibits bleomycininduced cellular senescence in murine lung fibroblasts
http://hdl.handle.net/2297/45342
http://hdl.handle.net/2297/4534273863637-22d2-4750-a3be-25cc369da4d0
| 名前 / ファイル | ライセンス | アクション |
|---|---|---|
AN00044397-125-1-2-13.pdf (2.0 MB)
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| Item type | 紀要論文 / Departmental Bulletin Paper(1) | |||||
|---|---|---|---|---|---|---|
| 公開日 | 2017-12-05 | |||||
| タイトル | ||||||
| タイトル | Sphingosine-1-phosphate receptor type 2 (S1P2) inhibits bleomycininduced cellular senescence in murine lung fibroblasts | |||||
| 言語 | ||||||
| 言語 | eng | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | fibroblasts | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | bleomycin | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | fibrosis | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | cellular senescence | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | sphingosine-1-phosphate | |||||
| キーワード | ||||||
| 主題Scheme | Other | |||||
| 主題 | S1P2 | |||||
| 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 | departmental bulletin paper | |||||
| 著者 |
Juanjuan, Zhao
× Juanjuan, Zhao× Okamoto, Yasuo× Takuwa, Yoh |
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| 書誌情報 |
金沢大学十全医学会雑誌 = Journal of the Juzen Medical Society 巻 125, 号 1, p. 2-13, 発行日 2016-03-01 |
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| ISSN | ||||||
| 収録物識別子タイプ | ISSN | |||||
| 収録物識別子 | 0022-7226 | |||||
| NCID | ||||||
| 収録物識別子タイプ | NCID | |||||
| 収録物識別子 | AN00044397 | |||||
| 出版者 | ||||||
| 出版者 | 金沢大学十全医学会 = The Juzen Medical Society Kanazawa University | |||||
| 抄録 | ||||||
| 内容記述タイプ | Abstract | |||||
| 内容記述 | The lysophospholipid mediator sphingosine-1-phosphate (S1P) exerts diverse biological activities including the regulation of leukocyte migration and vascular barrier integrity, suggesting that S1P signaling could be involved in inflammatory fibrotic diseases. Pulmonary fibrosis is a devastating disease characterized by fibroblast accumulation and extracellular matrix deposition in lungs, and bleomycin–induced pulmonary fibrosis is the most widely used experimental model. We studied the effects of the S1P–specific receptor S1P2 on the phenotypes of lung fibroblasts isolated from bleomycin- and saline-administered wild-type and S1P2–null (S1pr2-/-) mice. The lung fibroblasts from bleomycin-administered wild-type and S1pr2-/- mice failed to proliferate in the presence of serum, unlike fibroblasts from saline-administered mice. The fibroblasts from bleomycin-administered mice also showed the enlarged and flattened morphology compared with fibroblasts from control mice. Bleomycin administration increased the protein expression of the cell cycle inhibitor p16INK4a in fibroblasts and the number of senescence–associated β-galactosidase (SA-β-gal)-positive fibroblasts. In S1pr2-/- fibroblasts, bleomycin administration-induced increases in p16INK4a protein expression and SA–β-gal–positive cells were augmented. Furthermore, bleomycin increased mRNA expression of interleukin-6 and matrix metalloproteinases in S1pr2-/- fibroblasts compared with wild-type fibroblasts. In addition, the activation of Akt in response to platelet–derived growth factor and S1P was enhanced in S1pr2-/- fibroblasts compared with wild-type fibroblasts. These results indicate that S1P2 deletion enhances bleomycin administration–induced cellular senescence of lung fibroblasts, which may lead to inhibition of lung fibrosis through the mechanisms involving increased matrix metalloproteinases expression. Thus, S1P2 may be a novel therapeutic target for lung fibrosis. | |||||
| 著者版フラグ | ||||||
| 出版タイプ | VoR | |||||
| 出版タイプResource | http://purl.org/coar/version/c_970fb48d4fbd8a85 | |||||
