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. 2020 Jul 2;10:10868. doi: 10.1038/s41598-020-67730-y

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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The cross-talk model of osteoarthritis. We identified 12 subpopulations from OA synovia and 7 distinct chondrocyte subpopulations from OA articular cartilage. We predicted potential upstream regulators of chondrocyte gene expression during OA progression to infer molecular cross-talk networks between cartilage and synovium. Genes expressed by OA chondrocytes and identified as potential mediators of chondrocyte phenotypes in OA are indicated by blue solid dots with arrows; the preponderance of growth factors, such as TGFB among them, is consistent with upregulation of anabolic processes to maintain cartilage homeostasis in OA. However, genes identified as potential mediators of chondrocyte phenotypes in OA that were exclusively expressed (in > 1%) by synoviocytes but not by any of the chondrocyte subtypes are indicated by red solid dots with arrows; among these were genes for several key pro-inflammatory cytokines implicated in the pathogenesis of OA, including IL1A, IL1B, IL6 and TNF that were specifically expressed by inflammatory macrophages (I-Mϕ), dendritic cells (DC) or other synoviocytes. I-Mϕ and DC expressed HLA-DQA1, HLA-DQA2, OLR1 or TLR2; these cells appeared to be the primary cytokine producing cells.