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Article Open Access

Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts

  • Authors:
    • Lin Tao
    • Sichao Zhao
    • Zhengbo Tao
    • Kaicheng Wen
    • Siming Zhou
    • Wacili Da
    • Yue Zhu
  • View Affiliations / Copyright

    Affiliations: Department of Orthopedics, First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China
    Copyright: © Tao et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Pages: 1179-1186
    |
    Published online on: June 15, 2020
       https://doi.org/10.3892/mmr.2020.11228
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Abstract

Idiopathic scoliosis (IS) is a spinal 3‑dimensional deformity with an unknown cause. Melatonin is secreted by the pineal body and contributes to the occurrence and progression of IS. In our previous preliminary study, it was reported that high concentrations of melatonin can induce osteoblast apoptosis, thus acting as an IS treatment, but the mechanism of action is unknown. Therefore, the present study was performed to further investigate the possible mechanism underlying the efficacy of melatonin as a treatment for IS. The present results indicated that high concentrations of melatonin mediate endoplasmic reticulum stress (ERS)‑induced apoptosis in hFOB 1.19 cells, and this resulted in a significant and dose‑dependent increase in the expression of Septin4, as well as the expression levels of glucose‑regulated protein (GRP)78, GRP94 and cleaved caspase‑3. Furthermore, osteoblasts were overexpressed with Septin4 and the mechanism via which melatonin induces osteoblast ERS was demonstrated to be via the regulation of Septin4. In addition, it was indicated that cytoskeleton destruction, cell morphology changes and the decrease in the number of cells were aggravated after osteoblasts were overexpressed with Septin4, as indicated by phalloidin and DAPI staining. Collectively, the present results suggest that the Septin4 protein may be a target of ERS in melatonin‑induced osteoblast apoptosis, which is involved in bone metabolism diseases, thus providing novel evidence for clinical melatonin treatment of IS.
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Copy and paste a formatted citation
Spandidos Publications style
Tao L, Zhao S, Tao Z, Wen K, Zhou S, Da W and Zhu Y: Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts. Mol Med Rep 22: 1179-1186, 2020.
APA
Tao, L., Zhao, S., Tao, Z., Wen, K., Zhou, S., Da, W., & Zhu, Y. (2020). Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts. Molecular Medicine Reports, 22, 1179-1186. https://doi.org/10.3892/mmr.2020.11228
MLA
Tao, L., Zhao, S., Tao, Z., Wen, K., Zhou, S., Da, W., Zhu, Y."Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts". Molecular Medicine Reports 22.2 (2020): 1179-1186.
Chicago
Tao, L., Zhao, S., Tao, Z., Wen, K., Zhou, S., Da, W., Zhu, Y."Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts". Molecular Medicine Reports 22, no. 2 (2020): 1179-1186. https://doi.org/10.3892/mmr.2020.11228
Copy and paste a formatted citation
x
Spandidos Publications style
Tao L, Zhao S, Tao Z, Wen K, Zhou S, Da W and Zhu Y: Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts. Mol Med Rep 22: 1179-1186, 2020.
APA
Tao, L., Zhao, S., Tao, Z., Wen, K., Zhou, S., Da, W., & Zhu, Y. (2020). Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts. Molecular Medicine Reports, 22, 1179-1186. https://doi.org/10.3892/mmr.2020.11228
MLA
Tao, L., Zhao, S., Tao, Z., Wen, K., Zhou, S., Da, W., Zhu, Y."Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts". Molecular Medicine Reports 22.2 (2020): 1179-1186.
Chicago
Tao, L., Zhao, S., Tao, Z., Wen, K., Zhou, S., Da, W., Zhu, Y."Septin4 regulates endoplasmic reticulum stress and apoptosis in melatonin‑induced osteoblasts". Molecular Medicine Reports 22, no. 2 (2020): 1179-1186. https://doi.org/10.3892/mmr.2020.11228
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