Nickel Enhances Zinc-Induced Neuronal Cell Death by Priming the Endoplasmic Reticulum Stress Response
Joint Authors
Kawahara, Masahiro
Tanaka, Ken-ichiro
Kasai, Misato
Shimoda, Mikako
Shimizu, Ayane
Kubota, Maho
Source
Oxidative Medicine and Cellular Longevity
Issue
Vol. 2019, Issue 2019 (31 Dec. 2019), pp.1-13, 13 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2019-06-17
Country of Publication
Egypt
No. of Pages
13
Main Subjects
Abstract EN
Trace metals such as zinc (Zn), copper (Cu), and nickel (Ni) play important roles in various physiological functions such as immunity, cell division, and protein synthesis in a wide variety of species.
However, excessive amounts of these trace metals cause disorders in various tissues of the central nervous system, respiratory system, and other vital organs.
Our previous analysis focusing on neurotoxicity resulting from interactions between Zn and Cu revealed that Cu2+ markedly enhances Zn2+-induced neuronal cell death by activating oxidative stress and the endoplasmic reticulum (ER) stress response.
However, neurotoxicity arising from interactions between zinc and metals other than copper has not been examined.
Thus, in the current study, we examined the effect of Ni2+ on Zn2+-induced neurotoxicity.
Initially, we found that nontoxic concentrations (0–60 μM) of Ni2+ enhance Zn2+-induced neurotoxicity in an immortalized hypothalamic neuronal cell line (GT1-7) in a dose-dependent manner.
Next, we analyzed the mechanism enhancing neuronal cell death, focusing on the ER stress response.
Our results revealed that Ni2+ treatment significantly primed the Zn2+-induced ER stress response, especially expression of the CCAAT-enhancer-binding protein homologous protein (CHOP).
Finally, we examined the effect of carnosine (an endogenous peptide) on Ni2+/Zn2+-induced neurotoxicity and found that carnosine attenuated Ni2+/Zn2+-induced neuronal cell death and ER stress occurring before cell death.
Based on our results, Ni2+ treatment significantly enhances Zn2+-induced neuronal cell death by priming the ER stress response.
Thus, compounds that decrease the ER stress response, such as carnosine, may be beneficial for neurological diseases.
American Psychological Association (APA)
Tanaka, Ken-ichiro& Kasai, Misato& Shimoda, Mikako& Shimizu, Ayane& Kubota, Maho& Kawahara, Masahiro. 2019. Nickel Enhances Zinc-Induced Neuronal Cell Death by Priming the Endoplasmic Reticulum Stress Response. Oxidative Medicine and Cellular Longevity،Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1206548
Modern Language Association (MLA)
Tanaka, Ken-ichiro…[et al.]. Nickel Enhances Zinc-Induced Neuronal Cell Death by Priming the Endoplasmic Reticulum Stress Response. Oxidative Medicine and Cellular Longevity No. 2019 (2019), pp.1-13.
https://search.emarefa.net/detail/BIM-1206548
American Medical Association (AMA)
Tanaka, Ken-ichiro& Kasai, Misato& Shimoda, Mikako& Shimizu, Ayane& Kubota, Maho& Kawahara, Masahiro. Nickel Enhances Zinc-Induced Neuronal Cell Death by Priming the Endoplasmic Reticulum Stress Response. Oxidative Medicine and Cellular Longevity. 2019. Vol. 2019, no. 2019, pp.1-13.
https://search.emarefa.net/detail/BIM-1206548
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1206548