Other
13 Authors
- Guo W,
- Zhang D,
- Nakahara F,
- Wei Q,
- Alfieri A,
- Asada N,
- Brodin NP,
- Gao X,
- Xu C,
- Zimmerman SE,
- Guha C,
- Frenette PS,
- Mar JC
| First Author | Wei Q | Year | 2020 |
| Journal | Dev Cell | Volume | 53 |
| Issue | 5 | Pages | 503-513.e5 |
| PubMed ID | 32413329 | Mgi Jnum | J:290853 |
| Mgi Id | MGI:6437659 | Doi | 10.1016/j.devcel.2020.04.012 |
| Citation | Wei Q, et al. (2020) Snai2 Maintains Bone Marrow Niche Cells by Repressing Osteopontin Expression. Dev Cell 53(5):503-513.e5 |
| abstractText | Bone marrow (BM) mesenchymal stem and progenitor cells (MSPCs) are a critical constituent of the hematopoietic stem cell (HSC) niche. Previous studies have suggested that the zinc-finger epithelial-mesenchymal transition transcription factor Snai2 (also known as Slug) regulated HSCs autonomously. Here, we show that Snai2 expression in the BM is restricted to the BM stromal compartment where it regulates the HSC niche. Germline or MSPC-selective Snai2 deletion reduces the functional MSPC pool and their mesenchymal lineage output and impairs HSC niche function during homeostasis and after stress. RNA sequencing analysis revealed that Spp1 (osteopontin) expression is markedly upregulated in Snai2-deficient MSPCs. Genetic deletion of Spp1 in Snai2-deficient mice rescues MSPCs' functions. Thus, SNAI2 is a critical regulator of the transcriptional network maintaining MSPCs by the suppression of osteopontin expression. |
