Depletion of microenvironmental syndecan-2 impairs hematopoietic stem cell self-renewal and cytokine responses
Hagen, M. W.; Setiawan, N. J.; Wellington, R.; Woodruff, K. A.; Newman, C.; Billings, T. M.; Nazzaro, M. N.; Hadland, B.; Termini, C. M.
Show abstract
Syndecan-2 is a heparan sulfate proteoglycan highly enriched on murine bone marrow hematopoietic stem cells (HSCs) compared to terminally differentiated hematopoietic cells. Syndecan-2 binds growth factors via its heparan sulfate glycosaminoglycan chains to coordinate cell signaling. Knockdown of syndecan-2 reduces HSC self-renewal ability and promotes cell cycling via Cdkn1c. In this study, we analyzed the function of syndecan-2 expressed by bone marrow niche cells in hematopoiesis and HSC self-renewal. We determined that syndecan-2 is highly expressed by bone marrow mesenchymal stromal cells and moderately expressed by endothelial cells. To test the function of niche-expressed syndecan-2 in hematopoiesis, we generated transgenic mice depleted of Sdc2 in Lepr-targeted mesenchymal stromal cells (Sdc2{Delta}MSC mice) or Cdh5-targeted endothelial cells (Sdc2{Delta}EC mice). Loss of syndecan-2 from endothelial or mesenchymal stromal cells did not change bone marrow HSC frequencies or numbers. However, depletion of syndecan-2 from Lepr-targeted mesenchymal stromal cells, but not Cdh5-targeted endothelial cells, diminishes HSC self-renewal ability analyzed by competitive transplants into lethally irradiated mice. Ex vivo studies further show that HSCs co-cultured with HS-5 stromal cells depleted of SDC2 exhaust more rapidly than HSCs cultured with control HS-5 cells. Single-cell RNA sequencing analyses reveal that the depletion of Sdc2 from mesenchymal stromal cells significantly remodels the HSC transcriptome by enriching for pathways associated with excessive growth factor signaling. Together, our findings suggest that HSC self-renewal is supported by cell-extrinsic mechanisms enacted by syndecan-2 from the MSC niche, highlighting the importance of the niche proteoglycome in HSC functions. KEY POINTSO_LIThe heparan sulfate proteoglycan syndecan-2 expressed by mesenchymal stromal cells but not endothelial cells regulates HSC self-renewal C_LIO_LIDepletion of syndecan-2 from Lepr-targeted mesenchymal stromal cells remodels the hematopoietic stem cell transcriptional landscape C_LI
Matching journals
The top 6 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- Lfc/Arhgef2 regulates mitotic spindle orientation in hematopoietic stem and progenitor cells and is essential for productive hematopoiesis 97%
- Redundant mechanisms driven independently by RUNX1 and GATA2 for hematopoietic development 96%
- Unexpected redundancy of Gpr56 and Gpr97 during hematopoietic cell development and differentiation 96%
Similar papers in this journal
- Ubiquitous overexpression of CXCL12 confers radiation protection and enhances mobilization of hematopoietic stem and progenitor cells 96%
- JAK2V617F mutant megakaryocytes contribute to hematopoietic aging in a murine model of myeloproliferative neoplasm 95%
- CD146+CD107a+ Mesenchymal Stem/Stromal Cells with Signature Attributes Correlate to Therapeutic Potency as \"First Responders\" to Injury and Inflammation 93%
Similar papers in this journal
- Global transcriptomic profiling of the bone marrow stromal microenvironment during postnatal development, aging and inflammation 95%
- Fragmentation of macrophages during isolation confounds analysis of single cell preparations from mouse hematopoietic tissues 95%
- Allelic bias contributes to heterogeneous phenotypes of NK cell deficiency 95%
Similar papers in this journal
- CD99 Promotes Self-renewal in Hematopoietic Stem Cells and Leukemia Stem Cells by Regulating Protein Synthesis 97%
- Epo-IGF1R crosstalk expands stress-specific progenitors in regenerative erythropoiesis and myeloproliferative neoplasm 96%
- Hematopoietic recovery after transplantation is primarily derived from the stochastic contribution of hematopoietic stem cells 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.