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. 2017 Nov 2;8:244. doi: 10.1186/s13287-017-0696-x

Fig. 3.

Fig. 3

CD24 is a regulator for both resistance to IL-1β and higher proliferation in hiChondrocytes. (a) Loss of CD24 in hiChondrocytes increases the inflammatory response and dedifferentiation in the presence of IL-1β (10 ng/ml). In the absence of CD24 (shCD24), gene expression for IL6, CCL2, MMP3, and ADAMTS4 increases but decreases for the chondrogenic markers SOX9 and COL2A in the absence and presence of IL-1β. *, † both p < 0.01. (b) Loss of CD24 reduces Ki67 expression in proliferating chondrocytes. Representative immunofluorescence images for Ki67 (red) expression in chondrocytes, in the presence (nontarget control (NTC)) or absence of CD24 (shCD24). Nuclei (blue) are stained with DAPI. Scale bar, 100 μm. (c) Quantification of percentage of Ki67+ cells (average of 10 fields). Ki67+/total cell ratio in the presence (NTC) or absence (shCD24) of CD24 in adult chondrocytes, juvenile chondrocytes, and hiChondrocytes. Data represent two independent donors for each chondrocyte type and three replicate experiments