Upregulation of stromal cell-derived factor 1 (SDF-1) is associated with macrophage infiltration in renal ischemia-reperfusion injury.
Upregulation of stromal cell-derived factor 1 (SDF-1) is associated with macrophage infiltration in renal ischemia-reperfusion injury.
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基质细胞衍生因子 1 (SDF-1) 的上调与肾缺血再灌注损伤中的巨噬细胞浸润相关
DOI：
10.1371/journal.pone.0114564
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Cao C
中科院分区：
文献类型：
--
作者：
Wan X;Xia W;Gendoo Y;Chen W;Sun W;Sun D;Cao C
基质细胞衍生因子-1(SDF-1)是一种趋化和血管生成因子，介导多种组织的修复。由于巨噬细胞是缺血性肾损伤的重要因素，我们研究了SDF-1在大鼠缺血再灌注(I/R)损伤模型中的作用。雄性野生型(WT)(C57BL/6)小鼠在存在或不存在巨噬细胞耗竭的情况下，造成双侧I/R损伤或假手术(0.2ml/20~25g体重ip)。免疫组织化学方法检测巨噬细胞聚集情况。检测组织中SDF-1的表达水平(酶联免疫吸附试验)和SDF-1mRNA的表达(实时定量聚合酶链式反应)。免疫组织化学染色检测SDF-1的细胞定位。肾组织切片免疫荧光染色证实肾组织中巨噬细胞耗竭。SDF-1的产生在I/R损伤时升高，在巨噬细胞耗尽时显著增加。脑I/R损伤后，SDF-1阳性细胞首先出现在皮质，随后扩散至外髓。我们的研究表明，SDF-1在肾脏I/R过程中显著上调，我们推测SDF-1上调可能是I/R损伤过程中巨噬细胞的重要效应机制。
Stromal cell-derived factor-1(SDF-1) is a chemotactic and angiogenic factor that mediates the repair of various tissues. As macrophages are important contributors to ischemic kidney injury, we examine the role of SDF-1 in a rodent model of ischemia-reperfusion (I/R) injury. Male wild-type (WT) (C57BL/6) mice were subjected to bilateral I/R injury or sham operation in the presence or absence of macrophage depletion (liposomal clodronate [0.2 ml/20–25 g body weight i.p.]). Macrophage accumulation was assessed by immunohistochemistry. Tissue levels of SDF-1 (ELISA) and SDF-1 mRNA expression (real-time PCR) were measured. The cellular location of SDF-1 was assessed using immunohistochemical staining. Immunofluorescence staining of renal tissue sections confirmed macrophage depletion by liposomal clodronate. SDF-1 production was elevated in response to I/R injury and was significantly increased upon macrophage depletion. SDF-1 positive cells initially appeared initially in the cortex, and subsequently diffused to the outer medulla after I/R injury. Our study demonstrates that SDF-1 is significantly upregulated during renal I/R. We hypothesize that SDF-1 upregulation may be an important macrophage effector mechanism during I/R injury.
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影响因子：
13.6
作者：
Gröne, HJ;Cohen, CD;Nelson, PJ
通讯作者：
Nelson, PJ
DOI：
10.1007/s00417-008-0907-3
发表时间：
2008-12-01
影响因子：
2.7
作者：
Lai, Pinghong;Li, Tao;Tang, Shibo
通讯作者：
Tang, Shibo
影响因子：
82.9
作者：
Ceradini, DJ;Kulkarni, AR;Gurtner, GC
通讯作者：
Gurtner, GC
影响因子：
20.1
作者：
Tang YL;Zhu W;Cheng M;Chen L;Zhang J;Sun T;Kishore R;Phillips MI;Losordo DW;Qin G
通讯作者：
Qin G
影响因子：
15.9
作者：
Kollet, O;Shivtiel, S;Lapidot, T
通讯作者：
Lapidot, T