ババ ノブヤス
馬場 伸育 所属 川崎医科大学 医学部 基礎医学 免疫学 職種 講師 |
|
論文種別 | 原著 |
言語種別 | 英語 |
査読の有無 | 査読あり |
表題 | CCL11 promotes migration and proliferation of mouse neural progenitor cells. |
掲載誌名 | 正式名:Stem cell research & therapy 略 称:Stem Cell Res Ther ISSNコード:17576512/17576512 |
掲載区分 | 国外 |
巻・号・頁 | 8(1),pp.26 |
著者・共著者 | Feifei Wang, Nobuyasu Baba, Yuan Shen, Tatsuyuki Yamashita, Emi Tsuru, Masayuki Tsuda, Nagamasa Maeda, Yusuke Sagara |
発行年月 | 2017/02 |
概要 | BACKGROUND: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.METHODS: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.RESULTS: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.CONCLUSIONS: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. |
DOI | 10.1186/s13287-017-0474-9 |
PMID | 28173860 |