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. 1999 Jan 11;144(1):161–173. doi: 10.1083/jcb.144.1.161

Figure 4.

Figure 4

Altered endochondral bone formation in Col11a2-CDMP1 transgenic mice. (A) Histological sections of the humerus of normal (left) and 742- CDMP1-Int transgenic mice (right) at 14.5 d.p.c. (Top) Staining with Safranin O-fast green-iron hematoxylin of entire humerus. The transgenic mice (right) had the increased height of a zone of hypertrophic chondrocytes (h) compared to normal mice (left). In the transgenic mice, the primordial cartilage was wide and elbow joints were fused. (Bottom) Magnifications of the boxed regions of the distal part of the humerus in the top panels. The height of zones of proliferating chondrocytes was reduced in the transgenic mice. Note that arrays of chondrocytes at the bottom (asterisk) were different from those of chondrocytes located above in the transgenic mice. They were chondrocytes of the proximal part of the ulna. Hematoxylin and eosin staining. (B) Spatial expression of marker genes for endochondral bone formation in the forelimb of normal (left) and 742- CDMP1-Int transgenic (right) mice at 16.5 d.p.c. (Top row) Staining with Safranin O-fast green-iron hematoxylin. The skeletal components consist of proliferating and hypertrophic zones of chondrocytes and bone. In the transgenic mice, the carpals and distal part of the radius and ulna were completely fused and underwent endochondral bone formation as a single component. Semiserial sections were hybridized with cRNA probes of corresponding genes indicated on the left. Areas expressing Ihh (fourth row) and type X collagen (fifth row) mRNAs were remarkably enlarged in transgenic mice. r, resting chondrocytes; p, proliferating chondrocytes; h, hypertrophic chondrocytes. Scale bars, 100 μm.