CCL11 promotes migration and proliferation of mouse neural progenitor cells.
CCL11 promotes migration and proliferation of mouse neural progenitor cells.
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DOI：
10.1186/s13287-017-0474-9
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发表时间：
2017-02-07
影响因子：
7.5
通讯作者：
Sagara Y
中科院分区：
文献类型：
--
作者：
Wang F;Baba N;Shen Y;Yamashita T;Tsuru E;Tsuda M;Maeda N;Sagara Y
新生儿缺氧缺血在围产期引起大规模脑损伤，对中枢神经系统结构和功能的成熟产生长期影响。虽然神经祖细胞（NPC）迁移通过脑实质和家庭在啮齿动物脑损伤部位，分子机制是未知的。我们研究了新生儿缺氧缺血性脑损伤后趋化因子在介导NPC迁移中的作用。9日龄小鼠暴露于120分钟的缺氧后，单侧颈动脉闭塞。在小鼠脑提取物中定量趋化因子水平。使用胚胎和婴儿小鼠NPC进行迁移和增殖测定。新生儿缺氧缺血性脑损伤导致同侧病变，并扩展到皮质和纹状体区。NPC向受伤区域迁移，在那里检测到CC趋化因子的显着增加。体外研究表明，与重组小鼠CCL 11孵育的NPC促进迁移和增殖。CCR 3拮抗剂SB 297006可部分抑制上述作用。我们的数据暗示了CCL 11对小鼠NPC的重要作用。NPCs的有效激活可能为新生儿缺氧缺血性脑损伤的神经再生提供一种有希望的策略。本文的在线版本（doi：10.1186/s13287-017-0474-9）包含补充材料，可供授权用户使用。
Neonatal hypoxia-ischemia induces massive brain damage during the perinatal period, resulting in long-term consequences to central nervous system structural and functional maturation. Although neural progenitor cells (NPCs) migrate through the parenchyma and home in to injury sites in the rodent brain, the molecular mechanisms are unknown. We examined the role of chemokines in mediating NPC migration after neonatal hypoxic-ischemic brain injury. Nine-day-old mice were exposed to a 120-minute hypoxia following unilateral carotid occlusion. Chemokine levels were quantified in mouse brain extract. Migration and proliferation assays were performed using embryonic and infant mouse NPCs. The neonatal hypoxic-ischemic brain injury resulted in an ipsilateral lesion, which was extended to the cortical and striatal areas. NPCs migrated toward an injured area, where a marked increase of CC chemokines was detected. In vitro studies showed that incubation of NPCs with recombinant mouse CCL11 promoted migration and proliferation. These effects were partly inhibited by a CCR3 antagonist, SB297006. Our data implicate an important effect of CCL11 for mouse NPCs. The effective activation of NPCs may offer a promising strategy for neuroregeneration in neonatal hypoxic-ischemic brain injury. The online version of this article (doi:10.1186/s13287-017-0474-9) contains supplementary material, which is available to authorized users.
影响因子：
4.2
作者：
Kadam, S. D.;Mulholland, J. D.;McDonald, J. W.;Comi, A. M.
通讯作者：
Comi, A. M.