“…Recently, Risbud et al, suggested that hypoxia inducible factor 1a (HIF-1a) could be used to distinguish NP cells and articular chondrocytes [38]. NP cells uniquely expressed functionally active HIF-1a protein under normoxic conditions and only modestly increased their HIF-1a [36,45,46] vim Intermediate filament typically co-expressed with k19; expression reported in AF cells, large (''notochordal'') and small (''chondrocytic'') cells of the NP, and notochord cells; expression also documented in cartilage [3,7,21,22] anx3 Ca 2+ and phospholipid binding protein; influences membrane organization and traffic; regulates Ca 2+ currents across membranes and/or intracellular Ca 2+ concentrations [12] comp Extracellular matrix glycoprotein that can cross-link type-II collagen; found abundantly in articular cartilage; also identified in NP and AF [8,20,39] mgp Vitamin-K dependent protein found in bone and cartilage; expression up-regulated in endochondral bone formation, pathological calcification of cartilage, and immature and periosteal hypertrophic chondrocytes during fracture healing [2,15,16,23,24,33] transcriptional activity in a low-oxygen environment. In contrast, AF cells, chondrocytes and osteoblasts showed low-level expression of HIF-1a under normoxia, with significant protein induction at hypoxia.…”