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Fig. 3 | Arthritis Research & Therapy

Fig. 3

From: Molecular mechanisms underlying osteoarthritis development: Notch and NF-κB

Fig. 3

Crosstalk between Notch and NF-κB signalling pathways in regulation of OA development. Increase of Jag1 expression during OA progression may be due to activation of NF-κB signalling, as well as occurring in endothelial cells. The non-canonical NF-κB proteins p52 and RELB may enhance transcriptional activity of Notch-ICD and Rbpj, as seen in rheumatoid arthritis model mice. Among the identified downstream factors, proteinases and inflammation-related molecules are probably common mediators of both pathways. Adamts5 A disintegrin and metallopeptidase with thrombospondin type 1 motif 5, CaMKII calcium/calmodulin-dependent protein kinase II, Hes hairy and enhancer of split, HIF hypoxia-inducible factor, ICD intracellular domain, IHH indian hedgehog, IκB inhibitors of NF-κB, IKK inhibitors of NF-κB kinase, IL interleukin, IL1RL1IL-1 receptor-like 1, Jag Jagged, MMP matrix metalloproteinase, OA osteoarthritis, Rbpj recombination signal binding protein for Ig kappa J, Rela v-rel reticuloendotheliosis viral oncogene homologue A, VEGF vascular endothelial growth factor

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