CD163, a Hemoglobin/Haptoglobin Scavenger Receptor, After Intracerebral Hemorrhage: Functions in Microglia/Macrophages Versus Neurons
CD163, a Hemoglobin/Haptoglobin Scavenger Receptor, After Intracerebral Hemorrhage: Functions in Microglia/Macrophages Versus Neurons
复制标题
DOI：
10.1007/s12975-017-0535-5
复制
发表时间：
2017-12-01
影响因子：
6.9
通讯作者：
Xi, Guohua
中科院分区：
文献类型：
--
作者：
Garton, Thomas;Keep, Richard F.;Xi, Guohua
脑出血(ICH)后，血栓性因子会导致继发性脑损伤。尤其是在红血球分解过程中释放的血红蛋白，由于其含有含铁的血红素辅因子，一直是大量研究的焦点。当不与O2结合时，血红素结合的铁以亚铁(Fe2+)的状态存在，能够进行自由基化学反应，产生危险的活性氧物种。几项研究强调了出血性中风期间血红蛋白对神经元造成的损害，表明存在与血红蛋白相关的铁进入神经元并造成氧化损伤的途径[1-3]。虽然有几种已知的机制可以使游离铁和血红素进入细胞，但已知的血红蛋白摄取机制的数量有限。最具代表性的是CD163，长期以来被认为是单核/巨噬细胞的标志。最近的证据表明，CD163也可以在脑出血后的神经元群体中表达，这为神经元摄取血红蛋白提供了一种机制[2，4]。这篇评论讨论了CD163在脑出血后小胶质细胞/巨噬细胞中的潜在有益作用，并将它们与该受体在神经元中可能具有的潜在有害影响进行了比较。
Following intracerebral hemorrhage (ICH), clot-derived factors cause secondary brain damage. In particular, hemoglobin released during erythrolysis has been the focus of a large body of research due to its iron-containing heme cofactors. When not bound to O2, heme-bound iron exists in a ferrous (Fe2+) state capable of performing radical chemistry to create dangerous reactive oxygen species. Several studies have highlighted the hemoglobin-induced damage caused to neuronal populations during hemorrhagic stroke, suggesting the existence of pathways by which hemoglobin-associated iron can enter neurons and inflict oxidative injury [1–3]. While there are several known mechanisms by which free iron and heme can enter cells, the number of known hemoglobin uptake mechanisms is limited. The best characterized is CD163, long thought to be a marker of monocytes/macrophages. Recent evidence shows that CD163 can also be expressed in neuronal populations following ICH, providing a mechanism for hemoglobin uptake into neurons [2, 4]. This commentary discusses the potential beneficial roles of CD163 in microglia/macrophages after ICH and compares them to potentially detrimental effects the receptor may have in neurons.