Title |
Evidence for the role of connexin 43-mediated intercellular communication in the process of intracortical bone resorption via osteocytic osteolysis
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Published in |
BMC Musculoskeletal Disorders, April 2014
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DOI | 10.1186/1471-2474-15-122 |
Pubmed ID | |
Authors |
Shane A Lloyd, Alayna E Loiselle, Yue Zhang, Henry J Donahue |
Abstract |
Connexin 43 (Cx43) is the predominant gap junction protein in bone. Mice with a bone-specific deletion of Cx43 (cKO) have an osteopenic cortical phenotype. In a recent study, we demonstrated that cKO mice are resistant to bone loss induced by hindlimb suspension (HLS), an animal model of skeletal unloading. This protective effect occurred primarily as a result of lower osteoclast-mediated bone resorption. Interestingly, we also documented a significant increase in cortical osteocyte apoptosis and reduced sclerostin production. In the present study, we investigated whether osteocytic osteolysis - bone resorption by osteocytes within lacunae - is induced by HLS and the potential effect of Cx43 deficiency on this process during unloading. |
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