Cav1.3 is upregulated in osteoporosis rat model and promotes osteoclast differentiation from preosteoclast cell line RAW264.7.

J Cell Physiol 2019 Aug 11;234(8):12821-12827. Epub 2019 Feb 11.

Department of Rheumatism and Immunology, The First Affiliated Hospital Xi'an Jiaotong University, Xi'an, China.

Background: Osteoporosis (OP) is a systemic osteopathy with increased bone fragility and increased risk of fracture. Osteoclasts (OC) are the key target cells in the treatment of osteoporosis. We aimed to research the role of L-type calcium channel protein Cav1.3 in OC differentiation in this study.

Methods: OP rat model was established to detect the expression level of Cav1.3. Tartrate-resistant acid phosphatase assay was used to measure the differentiation of osteoclast during receptor activator of nuclear factor κ-Β ligand (RANKL)-induced osteoclasts formation. The expression of bone differentiation-related proteins were detected by western blot analysis.

Results: Cav1.3 is upregulated in OP rats. Knockdown of Cav1.3 inhibits the differentiation of RAW264.7. Cav1.3 regulates the cell differentiation and bone resorption of RAW264.7 during RANKL-induced osteoclasts formation, which is accompanied by upregulation of CaMK II, p-CERB, AP-1, NFATC1, and NF-κB.

Conclusion: Cav1.3 plays an important role in osteoporosis and the differentiation of osteoclast, which might be involved with the bone differentiation-related proteins.

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http://doi.wiley.com/10.1002/jcp.27937
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http://dx.doi.org/10.1002/jcp.27937DOI Listing
August 2019
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