Fig. 3: Ablating Hnrnpk in hypertrophic chondrocytes results in enhanced transdifferentiation potential. | Cell Death & Disease

Fig. 3: Ablating Hnrnpk in hypertrophic chondrocytes results in enhanced transdifferentiation potential.

From: Hnrnpk maintains chondrocytes survival and function during growth plate development via regulating Hif1α-glycolysis axis

Fig. 3

A Skeletal preparation of P0 (left panel) and P7 (right panel) WT and cCKO mice. Scale bar: 1 mm. B Quantification of limb length of P0 (top) and P7 (bottom) WT and cCKO mice. n = 3 biological replicates. C von Kassa staining of humerus of P0 and P7 WT and cCKO mice. Red arrow: excessive mineral bone in cCKO mice. Scale bar: 100 μm. D Immunostaining of Sp7 (left panel) and Cathepsin K (Ctsk) (right panel) of femur of P0 WT and cCKO mice (left panel) and the quantification of Sp7 and Ctsk positive cells (right panel). Dotted lines: boundary between hypertrophic zone and POC. n = 3 biological replicates. Scale bar: 100 μm. E Immunostaining of Sp7 of P0 Col10a1-Cre;Rosa26-tdTomato and Col10a1-Cre;Hnrnpkfl/fl;Rosa26-tdTomato. White boxes: magnification of metaphysis. White arrow: tdTomato and Sp7 double-positive cells. Scale bar: 100 μm. F Total quantity and ratio of single positive cells and double-positive cells in (E) of P0 WT and cCKO mice. Statistical analysis was exerted upon a ratio of double-positive cells between WT and cCKO mice. n = 3 biological replicates. p-value was calculated by two-tailed unpaired Student’s t-test. Data were shown as mean ± SD. *p < 0.05; **p < 0.01; ns: not significant.

Back to article page