Figure 3
Figure 3. Lack of host-derived adiponectin exacerbates myeloma pathogenesis. (A) Female age-matched adiponectin-deficient (KO) mice or WT littermate controls were inoculated with 5TGM1 myeloma cells. Tumor burden was measured by serum IgG2bκ ELISA. Data demonstrate tumor burden with respect to time from tumor inoculation. Days 0 to 15 are expanded in the right panel graph to demonstrate differences in tumor burden at early time points. (B) Representative images of tibiae of myeloma-bearing WT and adiponectin knockout mice. Osteolytic lesions through cortical bone were quantitated after micro-CT analysis. (C) Trabecular bone volume was quantitated by micro-CT analysis. (D) Bone formation rates were quantitated by dynamic histomorphometry. (E) Using immunohistochemistry, apoptotic myeloma cells in bone marrow were quantitated based on TUNEL positivity (see also supplemental Figure 2 and supplemental Table 2). Data are mean ± SEM. *P < .05, **P < .01, and ***P < .001, compared with WT (WT, n = 3; KO, n = 6).

Lack of host-derived adiponectin exacerbates myeloma pathogenesis. (A) Female age-matched adiponectin-deficient (KO) mice or WT littermate controls were inoculated with 5TGM1 myeloma cells. Tumor burden was measured by serum IgG2bκ ELISA. Data demonstrate tumor burden with respect to time from tumor inoculation. Days 0 to 15 are expanded in the right panel graph to demonstrate differences in tumor burden at early time points. (B) Representative images of tibiae of myeloma-bearing WT and adiponectin knockout mice. Osteolytic lesions through cortical bone were quantitated after micro-CT analysis. (C) Trabecular bone volume was quantitated by micro-CT analysis. (D) Bone formation rates were quantitated by dynamic histomorphometry. (E) Using immunohistochemistry, apoptotic myeloma cells in bone marrow were quantitated based on TUNEL positivity (see also supplemental Figure 2 and supplemental Table 2). Data are mean ± SEM. *P < .05, **P < .01, and ***P < .001, compared with WT (WT, n = 3; KO, n = 6).

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