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

Septin4 调节褪黑素诱导的成骨细胞中的内质网应激和细胞凋亡

阅读:5
作者:Lin Tao #, Sichao Zhao #, Zhengbo Tao #, Kaicheng Wen, Siming Zhou, Wacili Da, Yue Zhu

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.

特别声明

1、本文转载旨在传播信息,不代表本网站观点,亦不对其内容的真实性承担责任。

2、其他媒体、网站或个人若从本网站转载使用,必须保留本网站注明的“来源”,并自行承担包括版权在内的相关法律责任。

3、如作者不希望本文被转载,或需洽谈转载稿费等事宜,请及时与本网站联系。

4、此外,如需投稿,也可通过邮箱info@biocloudy.com与我们取得联系。