The role of CD36 in peripheral nerve remyelination after crush injury
The role of CD36 in peripheral nerve remyelination after crush injury
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DOI：
10.1046/j.1460-9568.2003.02711.x
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发表时间：
2003-06-01
影响因子：
3.4
通讯作者：
Sakoda, S
中科院分区：
文献类型：
--
作者：
Eto, M;Yoshikawa, H;Sakoda, S
我们先前证明，A类巨噬细胞清道夫受体I/II型的缺乏涉及坐骨神经挤压损伤后A类巨噬细胞清道夫受体I/II型敲除小鼠中巨噬细胞对降解髓鞘的延迟吞噬[Naba et al .（2000）Exp.神经醇，166，83-89]。为了阐明清道夫受体之一的CD 36的作用，在这里，我们造成挤压损伤的坐骨神经的CD 36基因敲除小鼠和研究挤压损伤后的髓鞘再生与A类巨噬细胞清道夫受体I/II型基因敲除小鼠相比。虽然我们以前报道了大量的洋葱球在A类巨噬细胞清道夫受体I/II型敲除小鼠在3周，洋葱球的数量是有限的，在CD 36敲除小鼠和野生型小鼠。在形态计量学上，与野生型小鼠相比，损伤后3周和6周，CD 36基因敲除小鼠的髓鞘再生严重延迟，巨噬细胞浸润到神经束中相当频繁。免疫组化结果显示，野生型小鼠巨噬细胞氧化磷脂酰胆碱单克隆抗体和油红O染色阳性，而CD 36基因敲除小鼠巨噬细胞氧化磷脂酰胆碱和中性脂质生成均阴性，提示CD 36基因敲除小鼠巨噬细胞氧化磷脂酰胆碱和中性脂质生成受到干扰。我们推测巨噬细胞的延迟吞噬和脂质从降解的髓鞘中再利用的缺陷与CD 36基因敲除小鼠中严重延迟的髓鞘再生和少量的洋葱球有关。
We previously demonstrated that the deficiency of class A macrophage scavenger receptor type I/II was involved in the delayed phagocytosis of degraded myelin by macrophages in class A macrophage scavenger receptor type I/II knockout mice after crush injury of the sciatic nerve [Naba et al . (2000) Exp. Neurol ., 166, 83-89]. In order to elucidate the role of CD36, one of the scavenger receptors, here we inflicted crush injury to the sciatic nerves of CD36 knockout mice and investigated the remyelination after crush injury in comparison with that of class A macrophage scavenger receptor type I/II knockout mice. Although we previously reported a lot of onion-bulbs in class A macrophage scavenger receptor type I/II knockout mice at 3 weeks, the number of onion-bulbs was limited both in CD36 knockout mice and wild-type mice. In the morphometry, the remyelination was seriously delayed, and the infiltrating macrophages into the nerve fascicles were quite frequent in CD36 knockout mice compared with wild-type mice at 3 and 6 weeks postinjury. The immunohistochemistry with the monoclonal antibody reacted with oxidized phosphatidylcholine and oil red O staining were positive in wild-type mice, but were negative in CD36 knockout mice, suggesting that the oxidation of phosphatidylcholine and the generation of neutral lipids in macrophages were disturbed in CD36 knockout mice. We hypothesize that the delayed phagocytosis by macrophages and the defect in reuse of lipids from degraded myelin are related to seriously delayed remyelination and a small number of onion-bulbs in CD36 knockout mice.