The adipokine lipocalin-2 in the context of the osteoarthritic osteochondral junction

Corrigendum: The adipokine lipocalin-2 in the context of the osteoarthritic osteochondral junction. Scientific Reports, 6, 30666. https://doi.org/10.1038/srep30666Obesity and osteoarthritis (OA) form a vicious circle in which obesity contributes to cartilage destruction in OA, and OA-associated sedentary behaviour promotes weight gain. Lipocalin-2 (LCN2), a novel adipokine with catabolic activities in OA joints, contributes to the obesity and OA pathologies and is associated with other OA risk factors. LCN2 is highly induced in osteoblasts in the absence of mechanical loading, but its role in osteoblast metabolism is unclear. Therefore, because osteochondral junctions play a major role in OA development, we investigated the expression and role of LCN2 in osteoblasts and chondrocytes in the OA osteochondral junction environment. Our results showed that LCN2 expression in human osteoblasts and chondrocytes decreased throughout osteoblast differentiation and was induced by catabolic and inflammatory factors; however, TGF-beta 1 and IGF-1 reversed this induction. LCN2 reduced osteoblast viability in the presence of iron and enhanced the activity of MMP-9 released by osteoblasts. Moreover, pre-stimulated human osteoblasts induced LCN2 expression in human chondrocytes, but the inverse was not observed. Thus, LCN2 is an important catabolic adipokine in osteoblast and chondrocyte metabolism that is regulated by differentiation, inflammation and catabolic and anabolic stimuli, and LCN2 expression in chondrocytes is regulated in a paracrine manner after osteoblast stimulation.The authors acknowledge Mr. Oliver Shaw for performing the English revision and the support of Dr. Esbrit's. The authors' research is supported by research grants from Fondo de Investigación Sanitaria funded by the Instituto de Salud Carlos III (PI12/00144, PI13/00570, CP15/00007, PI14/00016 and PIE13/00024). R.G. is funded by the Instituto de Salud Carlos III through a Miguel Servet programme. A.V. is the recipient of a fellowship from the Fundación Conchita Rábago. A.G.M. was funded by the Universidad Carlos III de Madrid (Spain). R.L. and O.G. were funded by the Instituto de Salud Carlos III. O.G. is a member of the RETICS Programme, RD12/0009/0008 Instituto de Salud Carlos III (ISCIII). The research is supported by research grant from FEDE