Negative regulation of ERK1/2 by PI3K is required for the protective effects of Pyropia yezoensis peptide against perfluorooctane sulfonate-induced endoplasmic reticulum stress

Oh,Jeong  Hwan; Kim,Eun‑Young; Choi,Youn  Hee; Nam,Taek‑Jeong

doi:10.3892/mmr.2017.6285

Negative regulation of ERK1/2 by PI3K is required for the protective effects of Pyropia yezoensis peptide against perfluorooctane sulfonate-induced endoplasmic reticulum stress

Authors:
- Jeong Hwan Oh
- Eun‑Young Kim
- Youn Hee Choi
- Taek‑Jeong Nam
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Affiliations: Cell Biology Laboratory, Institute of Fisheries Sciences, Pukyong National University, Busan 46041, Republic of Korea, Department of Marine Bio‑Materials and Aquaculture, Pukyong National University, Busan 48513, Republic of Korea
Published online on: March 3, 2017 https://doi.org/10.3892/mmr.2017.6285
Pages: 2583-2587
Copyright: © Oh et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Perfluorooctane sulfonate (PFOS) is a stable fluorosurfactant, which causes adverse effects in various organisms. The present study was designed to investigate the effects of Pyropia yezoensis peptide (PYP), a peptide comprised of 11 residues (ALEGGKSSGGG), on PFOS-induced endoplasmic reticulum (ER) stress in Chang cells. PFOS exposure (400 µM) for 24 h significantly decreased cell viability, which was upregulated by 250‑1,000 pg/ml PYP treatment. Exposure to PFOS also significantly increased expression of the ER stress response protein, glucose-regulated protein 78 (GRP78), and phosphorylation of extracellular signal‑regulated kinase 1/2 (ERK1/2). These elevations were significantly decreased by PYP (250 pg/ml), and, in particular, the PFOS‑induced GRP78 upregulation was decreased following treatment with 10 µM SL327, an ERK‑kinase inhibitor. However, PYP‑induced decreases in GRP78 expression and ERK1/2 phosphorylation were upregulated following treatment with LY294002 (20 µM), a phosphatidylinositol‑3 kinase (PI3K) inhibitor. PFOS-induced apoptosis was also significantly attenuated by PYP (250 pg/ml) treatment, and the PYP‑induced reduction in apoptosis was abolished by inhibition of PI3K. These findings indicate that negative regulation of ERK1/2 by PI3K is essential for the protective effects of PYP against PFOS-induced cell death, suggesting that PYP may be a candidate for therapeutic use.

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