Hematopoietic stem cells do not depend on N-cadherin to regulate their maintenance.
Hematopoietic stem cells do not depend on N-cadherin to regulate their maintenance.
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DOI：
10.1016/j.stem.2008.10.005
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发表时间：
2009-02-06
期刊：
影响因子：
23.9
通讯作者：
Morrison SJ
中科院分区：
文献类型：
--
作者：
Kiel MJ;Acar M;Radice GL;Morrison SJ
根据“成骨细胞生态位”模型，造血干细胞（hsc）是通过n-钙粘蛋白介导的与骨髓内皮成骨细胞的亲同源粘附来维持的。与此模型相反，我们无法检测到造血干细胞中N-cadherin的表达，并且大多数造血干细胞不定位于内皮表面。尽管如此，有人认为造血干细胞表达低水平的n -钙粘蛋白，调节造血干细胞的维持。为了验证这一点，我们在成年Mx-1-Cre+N-cadherinfl/−小鼠的造血干细胞和其他造血细胞中有条件地删除了N-cadherin。n -钙粘蛋白缺乏对造血干细胞维持或造血没有可检测到的影响。n -钙粘蛋白缺乏不影响骨髓细胞结构或谱系组成、集落形成祖细胞的数量、造血干细胞的频率、造血干细胞维持造血功能的能力，也不影响它们在原发性或继发性移植中重建辐照小鼠的能力。n -钙粘蛋白的丢失不会导致HSC的缺失。造血干细胞中N-cadherin的表达并不是生态位功能所必需的。
According to the “osteoblastic niche” model, hematopoietic stem cells (HSCs) are maintained by N-cadherin-mediated homophilic adhesion to osteoblasts at the bone marrow endosteum. In contrast to this model, we cannot detect N-cadherin expression by HSCs and most HSCs do not localize to the endosteal surface. It has nonetheless been suggested that HSCs express low levels of N-cadherin that regulate HSC maintenance. To test this we conditionally deleted N-cadherin from HSCs and other hematopoietic cells in adult Mx-1-Cre+N-cadherinfl/− mice. N-cadherin deficiency had no detectable effect on HSC maintenance or hematopoiesis. N-cadherin deficiency did not affect bone marrow cellularity or lineage composition, the numbers of colony-forming progenitors, the frequency of HSCs, the ability of HSCs to sustain hematopoiesis over time, or their ability to reconstitute irradiated mice in primary or secondary transplants. Loss of N-cadherin does not lead to HSC depletion. N-cadherin expression by HSCs is not necessary for niche function.
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