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 mRNAseq, 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-Embigin knockdown OM, confirmed that loss of these molecules significantly reduced OM ability 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 in vitro manipulations of stem cells.
[doi:10.25345/C5Z02ZK81]
[dataset license: CC0 1.0 Universal (CC0 1.0)]
Keywords: Osteomacs ; hematopoiesis ; osteoblasts ; megakaryocytes ; CD166 ; Embigin
Principal Investigators: (in alphabetical order) |
Amber L. Mosley, Indiana University School of Medicine, USA Edward Srour, Indiana University School of Medicine, United States |
Submitting User: | edoud |
Safa F. Mohamad, Roy El Koussa, Joydeep Ghosh, Rachel Blosser, Andrea Gunawan, Justin Layer, Chi Zhang, Sonali Karnik Utpal Davé, Melissa A. Kacena, Edward F. Srour.
Osteomacs promote maintenance of murine hematopoiesis through megakaryocyte-induced upregulation of Embigin and CD166.
Stem Cell Reports. 2024 (accepted) Stem-Cell-Reports-D-22-00477.
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