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. 2020 Apr 23;23:21–28. doi: 10.1016/j.jot.2020.03.007

Figure 3.

Figure 3

UCMSCs prohibited cartilage surface SFCs catabolism and preserved its number on the articular cartilage surface. (A) H&E staining showed typical elongated SFCs on the articular cartilage surface (arrows, upper panel). On the contrary, vehicle treated OA joint induced by MIA showed severe cartilage surface erosion and diminished SFCs (middle panel). UCMSCs administration moderately reserved the numbers of SFCs after MIA injection ​(lower panel). (Scale bars, 200 ​and 50 ​μm.) (B) Quantification of SFCs on the fixed cartilage area. ∗∗∗p＜ 0.001. (C) Effect of UCMSC-CM on SFCs' proliferation measured by CCK-8 assays. (D) and (E) Catabolism triggered by MIA treatment raise the Col-X and Bcl-2 gene expression, but conditioned media from UCMSCs could significantly downregulated those two catabolic genes. ∗∗∗∗p ＜ 0.0001, one-way repeated measures ANOVA, results are representative of at least three independent experiments and expressed as mean ​± ​standard deviation. H&E = haematoxylin and eosin; MIA = monosodium iodoacetate; SFCs = superficial layer cells; UCMSCs = umbilical cord–derived mesenchymal stem cells; UCMSCs-CM = UCMSCs-conditioned media.