Phosphatidylserine-specific receptor contributes to TGF-β production in macrophages through a MAP kinase, ERK
Phosphatidylserine-specific receptor contributes to TGF-β production in macrophages through a MAP kinase, ERK
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DOI：
10.1248/bpb.28.1707
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发表时间：
2005-09-01
影响因子：
2
通讯作者：
Aramaki, Y
中科院分区：
文献类型：
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作者：
Otsuka, M;Goto, K;Aramaki, Y
我们探讨了磷脂酰丝氨酸（PS）受体在经PS脂质体处理的巨噬细胞产生tgf - β中的作用。抗ps受体抗体与巨噬细胞的结合被ps脂质体特异性抑制。该抗体导致tgf - β的产生增加，并激活MAP激酶的成员ERK。但未观察到p38和JNK的活化。ERK抑制剂U0126完全阻止tgf - β的产生。在加入tgf - β中和抗体或U0126后，抗ps受体抗体对巨噬细胞功能和一氧化氮产生的抑制作用得以恢复。这些发现表明，tgf - β是ps脂质体产生的因子之一，而通过ps受体的ERK信号通路与巨噬细胞中tgf - β的产生密切相关。
We explored the involvement of the phosphatidylserine (PS)-receptor in the production of TGF-beta by macrophages treated with PS-liposomes. The binding of anti-PS-receptor antibody to macrophages was specifically inhibited by PS-liposomes. The antibody led to an increase in the production of TGF-beta, and also activated ERK, a member of the MAP kinase. But no activations in p38 and JNK were observed. ERK inhibitor, U0126 completely prevented TGF-beta production. On the addition of a TGF-beta neutralizing antibody or U0126, the inhibitory effect of the anti-PS-receptor antibody on macrophage function, nitric oxide production, was restored. These findings suggested that TGF-beta is one of factors produced by PS-liposomes, and the ERK signaling pathway via the PS-receptor is intimately involved in the production of TGF-beta in macrophages.