Involvement of phosphatidylinositol-3-kinase and ERK pathways in the production of TGF-β1 by macrophages treated with liposomes composed of phosphatidylserine
Involvement of phosphatidylinositol-3-kinase and ERK pathways in the production of TGF-β1 by macrophages treated with liposomes composed of phosphatidylserine
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DOI：
10.1016/j.febslet.2006.12.032
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发表时间：
2007-01-23
期刊：
影响因子：
3.5
通讯作者：
Aramaki, Yukihiko
中科院分区：
文献类型：
--
作者：
Otsuka, Masak;Negishi, Yoichi;Aramaki, Yukihiko
我们探讨了磷脂酰肌醇3-激酶（PI 3 K）和ERK途径参与由磷脂酰丝氨酸组成的脂质体（PS-脂质体）处理的巨噬细胞产生TGF-β 1。PS-脂质体激活Akt（PI 3 K信号级联的下游）和ERK（导致TGF-β 1的表达）。PI 3 K抑制剂LY 294002和wortmannin抑制PS脂质体处理后Akt和ERK的活化。这些抑制剂还抑制TGF-β 1的产生。此外，PS-脂质体通过PS特异性受体激活巨噬细胞以诱导TGF-β 1表达。这些发现表明，通过PS受体的PI 3 K-ERK信号传导途径密切参与调节巨噬细胞功能的TGF-β 1的产生。(c)2006年由Elsevier B. V.代表欧洲生物化学学会联合会出版。
We explored the involvement of phosphatidylinositol 3-kinase (PI3K) and ERK pathways in the production of TGF-beta 1 by macrophages treated with liposomes composed of phosphatidylserine (PS-liposomes). PS-liposomes activated Akt, downstream of the PI3K signal cascade, and ERK which led to the expression of TGF-beta 1. PI3K inhibitors, LY294002 and wortmannin, inhibited the activation of Akt and ERK following the treatment with PS-liposomes. These inhibitors also suppressed the production of TGF-beta 1. Furthermore, PS-liposomes activated macrophages to induce TGF-beta 1 expression through PS-specific receptors. These findings suggested that a PI3K-ERK signaling pathway via the PS-receptor is intimately involved in the production of TGF-beta 1 which regulates macrophage functions. (c) 2006 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.