Open Access

RIPK1 regulates the survival of human melanocytes upon endoplasmic reticulum stress

  • Authors:
    • Xuecheng Sun
    • Tao Wang
    • Bo Huang
    • Gaobo Ruan
    • Aie Xu
  • View Affiliations

  • Published online on: March 6, 2020     https://doi.org/10.3892/etm.2020.8575
  • Pages: 3239-3246
  • Copyright: © Sun et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Vitiligo is a common congenital or acquired disfiguring skin disorder. At present, endoplasmic reticulum (ER) stress has been identified to serve a critical role in the pathogenesis of vitiligo. Receptor‑interacting serine/threonine‑protein kinase 1 (RIPK1) is a protein serine/threonine kinase. The specific molecular mechanism of RIPK1 in human melanocytes upon ER stress remains to be determined. In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)‑induced ER stressed‑human melanocytes. Subsequently, to explore the role of RIPK1 in ER stress‑induced human melanocytes, human melanocytes were transfected with control or RIPK1 plasmids for 24 h and then treated with 3 µM TM for 48 h. Reverse transcription‑quantitative PCR and western blot analysis indicated that the expression levels of protein kinase R‑like endoplasmic reticulum kinase, eukaryotic translation initiation factor 2 subunit 1 and CCAAT‑enhancer‑binding protein homologous protein were significantly increased in the TM‑treated group compared with the controls. In addition, the effect of high RIPK1 expression on ER stress‑induced human melanocyte survival was studied. The present results indicated that TM inhibited cell viability and promoted apoptosis in human primary epidermal melanocytes. Western blot analysis demonstrated that the expression of Bax and caspase‑3 was upregulated and the expression of Bcl‑2 was downregulated in TM‑treated human melanocytes. The effects of TM on human melanocytes were reversed by RIPK1 overexpression. Therefore, RIPK1 overexpression may have an effect on the PI3K/AKT/mTOR signaling pathway in human melanocytes under ER stress. The results of the current study demonstrated that RIPK1 could protect human melanocytes from cell damage induced by ER stress by regulating the PI3K/AKT/mTOR and ER stress signaling pathways, thereby serving a protective role in the occurrence and development of vitiligo.

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May 2020
Volume 19 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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APA
Sun, X., Wang, T., Huang, B., Ruan, G., & Xu, A. (2020). RIPK1 regulates the survival of human melanocytes upon endoplasmic reticulum stress. Experimental and Therapeutic Medicine, 19, 3239-3246. https://doi.org/10.3892/etm.2020.8575
MLA
Sun, X., Wang, T., Huang, B., Ruan, G., Xu, A."RIPK1 regulates the survival of human melanocytes upon endoplasmic reticulum stress". Experimental and Therapeutic Medicine 19.5 (2020): 3239-3246.
Chicago
Sun, X., Wang, T., Huang, B., Ruan, G., Xu, A."RIPK1 regulates the survival of human melanocytes upon endoplasmic reticulum stress". Experimental and Therapeutic Medicine 19, no. 5 (2020): 3239-3246. https://doi.org/10.3892/etm.2020.8575