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Aluminum Chloride Induces Osteoblasts Apoptosis via Disrupting Calcium Homeostasis and Activating Ca2+/CaMKII Signal Pathway

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Abstract

Aluminum promotes osteoblast (OB) apoptosis. Apoptosis is induced by the disordered calcium homeostasis. Therefore, to investigate the relationship between Al-induced OB apoptosis and calcium homeostasis, calvarium OBs from neonatal rats (3–4 days) were cultured and exposed to 0.048-mg/mL Al3+ or 0.048-mg/mL Al3+ combined with 5 μM BAPTA-AM (OBs were pretreated with 5 μM BAPTA-AM for 1 h, then added 0.048 mg/mL Al3+), respectively. Then OB apoptosis rate, intracellular calcium ions concentration ([Ca2+]i), mRNA expression level of calmodulin (CaM), and protein expression levels of CaM and p-CaMKII in OBs were examined. The result showed that AlCl3 increased OB apoptosis rate, and [Ca2+]i and p-CaMKII expression levels and decreased CaM expression levels, whereas BAPTA-AM relieved the effects. These results proved that AlCl3 induced OB apoptosis by disrupting the intracellular Ca2+ homeostasis and activating the Ca2+/CaMKII signal pathway. Our findings can provide new insights for revealing the apoptosis mechanism of OBs exposed to AlCl3.

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Acknowledgment

The following are contract grant sponsors: National Science Foundation Project (contract grant number: 31372375) and Science and Technology Program of Heilongjiang Educational Bureau (contract grant number: C201425).

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Correspondence to Yanfei Li.

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Zheng Cao and Dawei Liu contributed equally to this study.

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Cao, Z., Liu, D., Zhang, Q. et al. Aluminum Chloride Induces Osteoblasts Apoptosis via Disrupting Calcium Homeostasis and Activating Ca2+/CaMKII Signal Pathway. Biol Trace Elem Res 169, 247–253 (2016). https://doi.org/10.1007/s12011-015-0417-1

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  • DOI: https://doi.org/10.1007/s12011-015-0417-1

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