Congenic Mice Confirm That Collagen X Is Required for Proper Hematopoietic Development

摘要: The link between endochondral skeletal development and hematopoiesis in the marrow was established collagen X transgenic (Tg) null (KO) mice. Disrupted function of X, a major hypertrophic cartilage matrix protein, resulted hematopoietic defects endochondrally derived tissues. Manifestation disease phenotype variable, ranging from perinatal lethality subset mice, to altered lymphopoiesis impaired immunity surviving To exclude contribution strain specific modifiers this variable manifestation skeleto-hematopoietic phenotype, C57Bl/6 DBA/2J congenic lines were established. Comparable manifestations confirmed that alterations are an inherent outcome disrupted function. Further, colony forming cell assays, complete blood count analysis, serum antibody ELISA, organ outgrowth studies all Tg KO mice implicated opportunistic infection as contributor severe phenotype. These data support model where ossification-specific contributes establishment niche at chondro-osseous junction.