Rescue of the skeletal phenotype in CasR-deficient mice by transfer onto the Gcm2 null background
J. Clin. Invest. Qisheng Tu, et al. 111:1029 doi:10.1172/JCI17054 [Go to this article.]

Figure 4
Nondecalcified histologic sections of the tibia of 1-week-old CasR- and Gcm2-deficient mice. Shown are group I controls (a–d), group II CasR-deficient mice (e–h), group III Gcm2-deficient mice (i–l), and group IV double homozygous CasR- and Gcm2-deficient mice (m–p). A toluidine blue–stained section of the growth plate (×125 in a, e, i, and m and ×250 in b, f, j, and n) shows a widened zone of hypertrophic chondrocytes in group II CasR-deficient mice that was corrected in group IV double homozygous CasR- and Gcm2-deficient mice, which were indistinguishable from group I and group III mice. A higher-power view of Goldner-stained sections (×500 in c, g, k, and o) of trabecular bone in secondary spongiosa. Excess osteoid is present in group II CasR^–/– mice (g) and resolution of hyperosteoidosis in group IV double knockout mice (o). In Goldner-stained sections, mineralized bone is blue and unmineralized osteoid is reddish-brown in color. The view under fluorescent light of Villanueva-stained sections of metaphysis (×500 in d, h, l, and p) showing the attenuation of calcein deposition in the primary and secondary spongiosa of group II CasR-deficient mice (h) is normalized in group IV double knockout mice (p).