Skeletogenesis and the Hematopoietic Niche

Defective Endochondral Ossification-Derived Matrix and Bone Cells Alter the Lymphopoietic Niche in Collagen X Mouse Models

“…Further, all ColX-Tg/KO mice have diminished B lymphopoiesis throughout life, aberrant serum cytokines and impaired immune responses [38][39][40]42]. Our studies linked these hematopoietic defects directly to ColX disruption at the COJ, and thus, were the first to implicate hypertrophic cartilage and the COJ as contributors to the lymphopoietic niche [39,43,45,46]. The purpose of this study was to identify which COJ cell type(s) from the ColX-Tg/KO mice were defective in hematopoietic support, and thus, were contributing to aberrant B lymphopoiesis.…”

“…In these mice, the function of ColX, the major hypertrophic cartilage matrix protein, is impaired either by transgenesis leading to dominant interference at the protein level [35][36][37], or by gene inactivation [35,[38][39][40][41][42][43]. We had reported that both the ColX-Tg and KO mice have similar structural changes at the chondroosseous junction (COJ), which represents the interface between the growth plate, trabecular bone, and the hematopoietic marrow.…”