Low peak bone mass and attenuated anabolic response to parathyroid hormone in mice with an osteoblast-specific deletion of connexin43

• DOI: 10.1242/jcs.03162
• Publication Date: 2006-09-20T02:02:10Z
• Authors: Dong Jin Chung; Charlles H. M. Ca...; Marcus Watkins; Joseph P. Stains; Min Young Chung; Vera Lucia Szejnfeld; Klaus Willecke; Martin Theis; Roberto Civitelli
• Keywords: Bone remodeling; Apposition; Peak bone mass; Teriparatide

Connexin43 (Cx43) is involved in bone development, but its role adult homeostasis remains unknown. To overcome the postnatal lethality of Cx43 null mutation, we generated mice with selective osteoblast ablation Cx43, obtained using a Cx43fl allele and 2.3-kb fragment alpha1(I) collagen promoter to drive Cre osteoblasts (ColCre). Conditionally osteoblast-deleted ColCre;Cx43-/fl show no malformations at birth, develop low peak mass remain osteopenic age, exhibiting reduced formation defective function. By both radiodensitometry histology, mineral content increased rapidly progressively Cx43+/fl after subcutaneous injection parathyroid hormone (PTH), an effect significantly attenuated mice, Cx43-/fl intermediate response. Attenuation PTH anabolic action was associated failure increase apposition rate response ColCre;Cx43-/fl, despite number, suggesting functional defect Cx43-deficient bone-forming cells. In conclusion, lack leads suboptimal acquisition mass, hinders PTH. represents potential target for modulation anabolism.