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Staphylococcal Protein A Promotes Osteoclastogenesis Through MAPK Signaling During Bone Infection

Overview
Journal J Cell Physiol
Specialties Cell Biology
Physiology
Date 2017 Feb 11
PMID 28185243
Citations 27
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Abstract

Bone infection is a common and serious complication in the orthopedics field, which often leads to excessive bone destruction and non-union. Osteoclast is the only type of cells which have the function of bone resorption. Its over activation is closely related to excessive bone loss. Staphylococcus aureus (S. aureus) is a major pathogen causing bone infection, which can produce a large number of strong pathogenic substances staphylococcal protein A (SPA). However, few studies were reported about the effects of SPA on osteoclastogenesis. In our study, we observed that S. aureus activated osteoclasts and promoted bone loss in bone infection specimens. Then, we investigated the effects of SPA on RANKL-induced osteoclastogenesis in vitro, the results revealed that SPA promoted osteoclastic differentiation and fusion, and enhanced osteoclastic bone resorption. In addition, we also showed that SPA upregulated the expression of NFATc1 and c-FOS through the activation of MAPK signaling to promote osteoclastogenesis. Our findings might help us better understand the pathogenic role of S. aureus in bone infection and develop new therapeutic strategies for infectious bone diseases.

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References
1.
Vaudaux P, Ferry T, Uckay I, Francois P, Schrenzel J, Harbarth S . Prevalence of isolates with reduced glycopeptide susceptibility in orthopedic device-related infections due to methicillin-resistant Staphylococcus aureus. Eur J Clin Microbiol Infect Dis. 2012; 31(12):3367-74. DOI: 10.1007/s10096-012-1705-8. View

2.
Qiao H, Wang T, Yu Z, Han X, Liu X, Wang Y . Structural simulation of adenosine phosphate via plumbagin and zoledronic acid competitively targets JNK/Erk to synergistically attenuate osteoclastogenesis in a breast cancer model. Cell Death Dis. 2016; 7:e2094. PMC: 4849151. DOI: 10.1038/cddis.2016.11. View

3.
Dou C, Zhang C, Kang F, Yang X, Jiang H, Bai Y . MiR-7b directly targets DC-STAMP causing suppression of NFATc1 and c-Fos signaling during osteoclast fusion and differentiation. Biochim Biophys Acta. 2014; 1839(11):1084-96. DOI: 10.1016/j.bbagrm.2014.08.002. View

4.
Wang Y, Liu X, Dou C, Cao Z, Liu C, Dong S . Staphylococcal protein A promotes osteoclastogenesis through MAPK signaling during bone infection. J Cell Physiol. 2017; 232(9):2396-2406. PMC: 5485048. DOI: 10.1002/jcp.25774. View

5.
Teitelbaum S, Ross F . Genetic regulation of osteoclast development and function. Nat Rev Genet. 2003; 4(8):638-49. DOI: 10.1038/nrg1122. View