STAT3 signaling within hepatocytes is required for anemia of inflammation in vivo
STAT3 signaling within hepatocytes is required for anemia of inflammation in vivo
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DOI：
10.1007/s00535-009-0159-y
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发表时间：
2010-02-01
影响因子：
6.3
通讯作者：
Hayashi, Norio
中科院分区：
文献类型：
--
作者：
Sakamori, Ryotaro;Takehara, Tetsuo;Hayashi, Norio
炎症性贫血通常见于慢性病患者，与血清铁降低有关。铁调素主要由肝细胞以STAT 3和/或SMAD依赖性方式产生，参与铁稳态。将松节油皮下注射到野生型小鼠或肝细胞特异性STAT 3-缺陷小鼠（L-STAT 3 KO）体内诱导炎症反应，结果表明，注射松节油后血清IL-6水平升高。它在野生型小鼠中激活了肝脏STAT 3，但在L-STAT 3 KO小鼠中没有。在慢性炎症中，野生型小鼠表现出血清铁水平降低和贫血，肝脏中铁调素水平上调。相比之下，L-STAT 3 KO小鼠没有表现出肝铁调素水平的增加或贫血。肝脏STAT 3通过铁调素的表达与炎症贫血的发展密切相关。肝脏通过STAT 3信号调节炎症性贫血。
Anemia of inflammation, commonly observed in patients with chronic diseases, is associated with decreased serum iron. Hepcidin, mainly produced by hepatocytes in a STAT3- and/or SMAD-dependent manner, is involved in iron homeostasis. What remains to be established is whether or not the hepatic IL-6/STAT3 signal has a role in anemia of inflammation in vivo.Turpentine oil was subcutaneously injected into wild-type mice or hepatocyte-specific STAT3-deficient mice (L-STAT3KO) to induce inflammation.Turpentine injection increased serum IL-6 levels. It activated liver STAT3 in wild-type mice, but not in L-STAT3KO mice. In chronic inflammation, wild-type mice showed decreased serum iron levels and anemia with up-regulation of hepcidin levels in the liver. In contrast, L-STAT3KO mice showed no increase in hepatic hepcidin levels or anemia.Liver STAT3 is critically involved in the development of anemia of inflammation via the expression of hepcidin. The liver regulates anemia of inflammation through STAT3 signaling.