Fig. 4

LOXL2 overexpression differentially regulates genes in osteoarthritis (OA) chondrocytes. Human articular chondrocytes from OA cartilage (HAC-OA) were transduced with adenoviruses for transient expression of LOXL2 (Ad-RFP-LOXL2) or Ad-RFP-empty vector (EV), and total RNA extracts were subjected to global gene expression analysis. LOXL2 overexpression in HAC-OA induced the upregulated gene signature (a) and the downregulated gene signature (b). c Statistical significance for differential gene expression. d Exogenous LOXL2 expression increased anabolic markers in HAC-OA chondrocytes, whereas genes related to chondrocyte hypertrophy and catabolic markers were not changed as validated by RT-qPCR (e) (*P < 0.001; Student’s t test). LOXL2 transduction increased the expression of collagen type II α1 (COL2A1) (P = 0.063), Sex determining region Y-box containing gene 9 (SOX9) (P = 0.002), and aggrecan (ACAN) (P = 0.003). NPPC natriuretic peptide C, CSPG chondroitin sulfate proteoglycan, GDF5 growth differentiation factor 5, TGFB3 transforming growth factor B3, IGFBP3 insulin-like growth factor binding protein, CABP5 calcium binding protein 5, SFRP1 secreted frizzled-related protein 1, TOBP1 topoisomerase II binding protein 1, VCAM1 vascular cell adhesion molecule 1, E2F8 E2F transcription factor 8, DKK1 Dickkopf WNT signaling inhibitor 1, CCNE2 cyclin E2, TPX microtubule-associated homolog, NAA N(alpha)-acetyltransferase, FDR false discovery rate, MMP matrix metalloproteinase