GSK-3β-mediated regulation of cadmiuminduced cell death and survival

• Autorzy: Kim S. , Cheon H. , Kim S.M. , Kim Y.Y.
• Języki publikacji: EN

Abstrakty

EN

Background: Previous studies indicated that cadmium (Cd) increases PI3-kinase/Akt phosphorylation, resulting in an alteration in GSK-3β activity. However, the mechanism of Cd-induced endoplasmic reticulum (ER) stress in neuronal cells has yet to be studied in needs further elucidation. We examined the role of GSK-3β in Cd-induced neuronal cell death and the related downstream signaling pathways. Methods: SH-SY5Y human neuroblastoma cells were treated with 10 or 20 μM BAPTA-AM and 1 μM wortmannin for 30 min and then incubated with 25 μM Cd for 12 h. Apoptotic cells were visualized via DAPI and PI staining. Data were evaluated with one-way analysis of variance (ANOVA) followed by Student’s t-test. Data are expressed as the means ± SD of experiments performed at least three times. Results: Treatment of human neuronal SH-SY5Y cells with Cd induced ER, stress as evidenced by the increased expression of GRP78, which is a marker of ER stress. Cd exposure significantly increased the phosphorylation of Akt at thr308 and ser473 and that of GSK-3β at ser9 in a time-dependent manner, while the total protein levels of GSK-3β and Akt did not change. Cd-induced apoptosis was higher in GSK-3β-knockdown cells than in normal cells. Conclusions: Our data suggest that Akt/GSK-3β signaling activated by Cd is involved in neuronal cell surviva

• Wydawca: -
• Czasopismo: Cellular and Molecular Biology Letters
• Rocznik: 2018
• Tom: 23
• Opis fizyczny: p.1-10,fig.,ref.

Twórcy

autor

Kim S.

• Division of Brain Diseases, Center for Biomedical Science, National Institute of Health, Center for Disease Control & Prevention, Osong Health Technology Administration Complex, 187, Osongsaengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju-si, South Korea

autor

Cheon H.

• Division of Brain Diseases, Center for Biomedical Science, National Institute of Health, Center for Disease Control & Prevention, Osong Health Technology Administration Complex, 187, Osongsaengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju-si, South Korea

autor

Kim S.M.

• Division of Brain Diseases, Center for Biomedical Science, National Institute of Health, Center for Disease Control & Prevention, Osong Health Technology Administration Complex, 187, Osongsaengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju-si, South Korea

autor

Kim Y.Y.

• Division of Biobank for Health Sciences, Center for Genome Science, National Institute of Health, Center for Disease Control & Prevention, 200 Osongsaengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju-si, South Korea

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Identyfikatory

DOI

10.1186/s11658-018-0076-2