Maintenance of hematopoietic stem cell (HSC) function in the niche is an orchestrated event. Osteomacs (OM) are key cellular components of the niche. Previously, we documented that osteoblasts, OM, and megakaryocytes interact to promote hematopoiesis. Here, we further characterize OM and identify megakaryocyte-induced mediators that augment the role of OM in the niche. Single-cell mRNA-seq, mass spectrometry, and CyTOF examination of megakaryocyte-stimulated OM suggested that upregulation of CD166 and Embigin on OM augment their hematopoiesis maintenance function. CD166 knockout OM or shRNA- knockdown OM confirmed that the loss of these molecules significantly reduced the ability of OM to augment the osteoblast-mediated hematopoietic-enhancing activity. Recombinant CD166 and Embigin partially substituted for OM function, characterizing both proteins as critical mediators of OM hematopoietic function. Our data identify Embigin and CD166 as OM-regulated critical components of HSC function in the niche and potential participants in various manipulations of stem cells.

中文翻译：

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Osteomacs 通过巨核细胞诱导的 Embigin 和 CD166 上调促进小鼠造血功能的维持

维持微环境中的造血干细胞（HSC）功能是一个精心策划的事件。 Osteomacs (OM) 是该利基的关键细胞成分。之前，我们记录了成骨细胞、OM 和巨核细胞相互作用以促进造血。在这里，我们进一步表征了 OM 并确定了巨核细胞诱导的介质，这些介质增强了 OM 在生态位中的作用。巨核细胞刺激的 OM 的单细胞 mRNA-seq、质谱和 CyTOF 检查表明，OM 上 CD166 和 Embigin 的上调增强了其造血维持功能。 CD166 敲除 OM 或 shRNA 敲除 OM 证实，这些分子的丢失显着降低了 OM 增强成骨细胞介导的造血增强活性的能力。重组 CD166 和 Embigin 部分取代了 OM 功能，将这两种蛋白描述为 OM 造血功能的关键介质。我们的数据表明 Embigin 和 CD166 是 OM 调节的 HSC 功能的关键组成部分，也是各种干细胞操作的潜在参与者。