| First Author | Sweeney E | Year | 2010 |
| Journal | PLoS One | Volume | 5 |
| Issue | 3 | Pages | e9518 |
| PubMed ID | 20209091 | Mgi Jnum | J:158698 |
| Mgi Id | MGI:4439445 | Doi | 10.1371/journal.pone.0009518 |
| Citation | Sweeney E, et al. (2010) Congenic mice confirm that collagen X is required for proper hematopoietic development. PLoS One 5(3):e9518 |
| abstractText | The link between endochondral skeletal development and hematopoiesis in the marrow was established in the collagen X transgenic (Tg) and null (KO) mice. Disrupted function of collagen X, a major hypertrophic cartilage matrix protein, resulted in skeletal and hematopoietic defects in endochondrally derived tissues. Manifestation of the disease phenotype was variable, ranging from perinatal lethality in a subset of mice, to altered lymphopoiesis and impaired immunity in the surviving mice. To exclude contribution of strain specific modifiers to this variable manifestation of the skeleto-hematopoietic phenotype, C57Bl/6 and DBA/2J collagen X congenic lines were established. Comparable disease manifestations confirmed that the skeleto-hematopoietic alterations are an inherent outcome of disrupted collagen X function. Further, colony forming cell assays, complete blood count analysis, serum antibody ELISA, and organ outgrowth studies established altered lymphopoiesis in all collagen X Tg and KO mice and implicated opportunistic infection as a contributor to the severe disease phenotype. These data support a model where endochondral ossification-specific collagen X contributes to the establishment of a hematopoietic niche at the chondro-osseous junction. |
