The chemokine CXCL16 induces migration and invasion of glial precursor cells via its receptor CXCR6
The chemokine CXCL16 induces migration and invasion of glial precursor cells via its receptor CXCR6
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DOI：
10.1016/j.mcn.2008.03.009
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发表时间：
2008-09-01
影响因子：
3.5
通讯作者：
Mentlein, Rolf
中科院分区：
文献类型：
--
作者：
Hattermann, Kirsten;Ludwig, Andreas;Mentlein, Rolf
趋化因子与大脑的发育和炎症过程有关。跨膜趋化因子CXCL16在脑内皮细胞和反应性星形胶质细胞中产生，并通过脱落释放。其受体CXCR6在出生后6天的大脑发育过程中被检测到，在神经干细胞分化的神经胶质前体细胞和a2b5阳性的神经胶质前细胞系中发现。可溶性cxcl16刺激它们可诱导pi3激酶/Akt和Erk通路，从而激活转录因子AP-1。作为生物反应，可溶性CXCL16上调其自身受体，增加细胞增殖，在伤口愈合和球体对抗试验中刺激细胞迁移。脱落酶抑制剂和cxcl16抗体可阻断cxcr6阳性胶质细胞向表达cxcl16的球体的侵袭。由于CXCL16是由炎症、神经变性、缺血和恶性转化部位的细胞因子诱导的，它应该吸引cxcr6阳性的胶质前体细胞，增强其侵袭和增殖，从而促进星形胶质细胞形成。(C) 2008爱思唯尔公司版权所有。
Chemokines are implicated in developmental and inflammatory processes in the brain. The transmembrane chemokine CXCL16 is produced in brain endothelial and reactive astroglial cells and released by shedding. Its receptor CXCR6 is detected during brain development highest at postnatal day 6, found in glial precursor cells differentiated from neural stem cells and in an A2B5-positive glial precursor cell line. Their stimulation by soluble CXCL 16 induces the PI3-kinase/Akt and Erk pathways resulting in the activation of the transcription factor AP-1. As biological responses, soluble CXCL16 upregulates its own receptor, increases cell proliferation, stimulates cell migration in wound-healing and in spheroid confrontation assays. Invasion of CXCR6-positive glial cells into CXCL16-expressing spheroids can be blocked by sheddase inhibitors and CXCL16-antibody. Since CXCL16 is induced by cytokines at sites of inflammation, neurodegeneration, ischemia and malignant transformation, it should attract CXCR6-positive glial precursor cells, enhance their invasion and proliferation and thus favor astrogliosis. (C) 2008 Elsevier Inc. All rights reserved.