The class D scavenger receptor CD68 contributes to mouse chronic liver injury
The class D scavenger receptor CD68 contributes to mouse chronic liver injury
复制标题
D类清道夫受体CD68导致小鼠慢性肝损伤
DOI：
10.1007/s12026-018-9002-y
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发表时间：
2018-05
影响因子：
4.4
通讯作者：
Liying Li
中科院分区：
文献类型：
--
作者：
Le Yang;Lin Yang;Chengbin Dong;Liying Li
表达于单核细胞/巨噬细胞上的清道夫受体在许多致病过程中起核心作用。在这里，我们研究了D类清道夫受体（CD 68）在慢性肝损伤中骨髓来源的单核细胞/巨噬细胞（BMPs）中的作用。采用qRT-PCR方法分析了两种肝损伤模型（蛋氨酸胆碱缺乏高脂（MCDHF）和四氯化碳（CCl 4））中多种清道夫受体的表达模式。通过流式细胞术分析、免疫荧光和qRT-PCR表征CD 68表达。采用选择性单核细胞/巨噬细胞毒物氯化钆（GdCl 3）在体外和体内分析CD 68的功能。在检测的7种清道夫受体（CD 68、CD 36、CD 204、MARCO、LOX 1、SREC和CD 163）中，CD 68的mRNA表达最高，并在慢性肝损伤的整个阶段持续升高，因此引起了我们的关注。在损伤的肝脏中，募集的CD 68 +BMM的百分比显著增加，沿着发展中的纤维化间隔排列，而CD 68 +KC的比例与对照小鼠相比保持不变。体外培养的BMM中CD 68高表达，并且在GdCl 3存在下，巨噬细胞吞噬和凋亡触发CD 68减少。GdCl 3可降低损伤肝脏中CD 68 +BMM的募集和CD 68 mRNA的表达，从而减轻肝脏炎症和纤维化。总之，清道夫受体CD 68在小鼠慢性肝损伤中起着关键作用，这对于设计抗纤维化疗法具有重要意义。
Scavenger receptors, which are expressed on monocyte/macrophages, play a central role in many pathogenic processes. Here, we examined the role of the class D scavenger receptor (CD68) in bone marrow-derived monocyte/macrophages (BMMs) in chronic liver injury. The expression pattern of multiple scavenger receptors in two liver injury models (methionine-choline-deficient and high fat (MCDHF), carbon tetrachloride (CCl4)) were analyzed by qRT-PCR. CD68 expression was characterized by flow cytometric analysis, immunofluorescence, and qRT-PCR. A selective monocyte/macrophage toxicant, gadolinium chloride (GdCl3) was applied to analyze the function of CD68 in vitro and in vivo. Among the seven examined scavenger receptors (CD68, CD36, CD204, MARCO, LOX1, SREC, and CD163), the mRNA expression of CD68 first got uppermost and continuously increased throughout the entire stage of chronic liver injury, thus attracting our attention. In the injured liver, the percentage of recruited CD68+BMM increased notably, aligning along the developing fibrotic septa, while the proportion of CD68+KC stayed the same compared with that of control mice. In vitro CD68 was highly expressed in primary cultured BMM, and CD68 reduction was triggered by macrophage phagocytosis and apoptosis in the presence of GdCl3. In the damaged liver, the recruitment of CD68+BMM and CD68 mRNA expression were reduced by GdCl3administration, leading to the attenuation of liver inflammation and fibrosis. Altogether, scavenger receptor CD68 plays a key role in mouse chronic liver injury, which has important implications for the design of anti-fibrotic therapies.
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影响因子：
13.5
作者：
Sica, Antonio;Invernizzi, Pietro;Mantovani, Alberto
通讯作者：
Mantovani, Alberto
影响因子：
4.4
作者：
Sun, Li-Xin;Lin, Zhi-Bin;Duan, Xin-Suo
通讯作者：
Duan, Xin-Suo
影响因子：
30.5
作者：
通讯作者：
--
影响因子：
--
作者：
А. Э. Гомбожапова;Ю. В. Роговская;М. С. Ребенкова;Ю. Г. Кжышковская;В. В. Рябов-В.
通讯作者：
А. Э. Гомбожапова;Ю. В. Роговская;М. С. Ребенкова;Ю. Г. Кжышковская;В. В. Рябов-В.
DOI：
10.1073/pnas.93.25.14833
发表时间：
1996-12-10
影响因子：
11.1
作者：
Ramprasad, MP;Terpstra, V;Steinberg, D
通讯作者：
Steinberg, D