Fetal liver hematopoietic stem cell niches associate with portal vessels.
Fetal liver hematopoietic stem cell niches associate with portal vessels.
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DOI：
10.1126/science.aad0084
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发表时间：
2016-01-08
期刊：
影响因子：
--
通讯作者：
Frenette PS
中科院分区：
文献类型：
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作者：
Khan JA;Mendelson A;Kunisaki Y;Birbrair A;Kou Y;Arnal-Estapé A;Pinho S;Ciero P;Nakahara F;Ma'ayan A;Bergman A;Merad M;Frenette PS
尽管骨髓中造血干细胞（HSC）小生境的细胞基础已被表征，但胎肝（FL）小生境的性质尚未阐明。我们发现巢蛋白+NG 2+周细胞与门脉血管相关，形成促进HSC扩张的小生境。Nestin+ NG 2+细胞和HSC在发育过程中随着门脉血管、脐静脉分支的分形分支模式而缩放。在出生时脐带入口关闭后，门静脉血管经历从Neuropilin-1+Ephrin-B2+动脉到EphB 4+静脉表型的转变，这与门静脉周围Nestin+ NG 2+细胞的损失和HSC从门静脉血管移出有关。这些数据支持一个模型，其中HSC对门静脉周围血管生态位滴定，胎盘循环使其具有分形样组织。
Whereas the cellular basis of the hematopoietic stem cell (HSC) niche in the bone marrow has been characterized, the nature of the fetal liver (FL) niche is not yet elucidated. We show that Nestin+NG2+ pericytes associate with portal vessels, forming a niche promoting HSC expansion. Nestin+NG2+ cells and HSCs scale during development with the fractal branching patterns of portal vessels, tributaries of the umbilical vein. After closure of the umbilical inlet at birth, portal vessels undergo a transition from Neuropilin-1+Ephrin-B2+ artery to EphB4+ vein phenotype, associated with a loss of periportal Nestin+NG2+ cells and emigration of HSCs away from portal vessels. These data support a model in which HSCs are titrated against a periportal vascular niche with a fractal-like organization enabled by placental circulation.