Macrophage involvement in the kidney repair phase after ischaemia/reperfusion injury
Macrophage involvement in the kidney repair phase after ischaemia/reperfusion injury
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DOI：
10.1002/path.2259
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发表时间：
2008-01-01
影响因子：
7.3
通讯作者：
Sola, A.
中科院分区：
文献类型：
--
作者：
Vinuesa, E.;Hotter, G.;Sola, A.
巨噬细胞浸润是肾缺血/再灌注损伤早期的共同特征。事实上，它通常被认为是该阶段组织损伤的原因，尽管它也可以导致其他阶段的组织修复。为了确定巨噬细胞是否直接参与肾缺血/再灌注的促炎和损伤过程之后的修复/晚期阶段，我们使用了两种基于巨噬细胞耗竭的不同方法。首先，我们在先前用氯膦酸盐脂质体治疗的小鼠中产生肾缺血。其次，在再灌注期间，我们在处死前24小时将RAW 264.7重新注射到巨噬细胞耗尽的小鼠。结果表明，再生，评价stathmin和PCNA标记，是巨噬细胞依赖性的：它被阻止时，巨噬细胞消耗挑起和恢复与巨噬细胞重新注射。细胞因子谱揭示了炎症环境对肾修复的影响：促炎细胞因子（MCP-1，MIP-1 α）在再灌注早期增加，与低再生一致，抗炎细胞因子IL-10在再生更明显的再灌注较长时间内增加。我们得出结论，巨噬细胞诱导缺血/再灌注后的肾再生，这取决于炎症环境。版权所有（c）2007大不列颠和爱尔兰病理学会。出版社：John Wiley & Sons，Ltd
Macrophage infiltration is a common feature of the early phase of renal ischaemia/reperfusion injury. Indeed, it is generally regarded as the cause of tissue injury in this phase, although it is also clear that it can lead to tissue repair in other phases. In order to ascertain whether macrophages are directly involved in the repair/late phase, which follows the pro-inflammatory and injury process of renal ischaemia/reperfusion, we used two different approaches based on macrophage depletion. Firstly, we produced renal ischaemia in mice that were previously treated with clodronate liposome. Secondly, during reperfusion we re-injected RAW 264.7 to macrophage-depleted mice 24 h prior to sacrifice. The results showed that regeneration, as evaluated by stathmin and PCNA markers, was macrophage-dependent: it was blocked when macrophage depletion was provoked and recovered with macrophage re-injection. The cytokine profile revealed the influence of the inflammatory environment on kidney repair: pro-inflammatory cytokines (MCP-1, MIP-1 alpha) increased during the early stages of reperfusion, coinciding with low regeneration, and the anti-inflammatory cytokine IL-10 increased during the longer periods of reperfusion when regeneration was more evident. We conclude that macrophages induce renal regeneration after ischaemia/reperfusion, depending on the inflammatory milieu. Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.