ANGIOTENSINOGEN PRODUCTION BY RAT HEPATOMA-CELLS IS STIMULATED BY B-CELL STIMULATORY FACTOR-II INTERLEUKIN-6
ANGIOTENSINOGEN PRODUCTION BY RAT HEPATOMA-CELLS IS STIMULATED BY B-CELL STIMULATORY FACTOR-II INTERLEUKIN-6
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DOI：
10.1016/0014-5793(89)81150-0
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发表时间：
1989-02-13
期刊：
影响因子：
3.5
通讯作者：
OKAMOTO, H
中科院分区：
文献类型：
--
作者：
ITOH, N;MATSUDA, T;OKAMOTO, H
血管紧张素原已被确定为急性期反应物之一。体外研究是使用H35肝癌细胞系来鉴定导致肝脏中血管紧张素原合成增加的细胞因子的种类。通过加入10− 7 M地塞米松，H35细胞的血管紧张素原分泌最大增加4倍。在此条件下，血管紧张素原分泌进一步被B细胞刺激因子2/白细胞介素-6（IL-6，50 U/ml）刺激，但不被白细胞介素-1或干扰素-α刺激。在不存在糖皮质激素的情况下，IL-6不影响H35细胞的血管紧张素原分泌，表明糖皮质激素的存在是IL-6刺激活性所必需的。这些表明，IL-6是急性炎症期间肝脏血管紧张素原合成增加的介体。
Angiotensinogen has been identified as one of the acute‐phase reactants. In vitro studies were carried out using the Reuber H35 hepatoma cell line to identify the species of cytokines contributing to the increased synthesis of angiotensinogen in the liver. Angiotensinogen secretion by H35 cells was maximally increased 4‐fold by the addition of 10−7M dexamethasone. Under this condition, angiotensinogen secretion was further stimulated by B cell stimulatory factor 2/interleukin‐6 (IL‐6, 50 U/ml), but not by interleukin‐1 or interferon‐α. In the absence of glucocorticoid, IL‐6 did not affect angiotensinogen secretion by H35 cells, indicating that the presence of glucocorticoid is required for the stimulatory activity of IL‐6. These suggest that IL‐6 is a mediator responsible for the increased synthesis of angiotensinogen in the liver during acute inflammation.