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, Jung‐Hwa; Kim, Eun Young; Choi, Youn Hee; Nam, Taek‐Jeong

doi:10.3892/mmr.2017.6285

Cited by 6 publications

(4 citation statements)

References 24 publications

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“…The MAPK pathway is involved in endoplasmic reticulum stress, cell proliferation, cell cycle arrest, and autophagy [ 32 ]. In addition, PFOS can induce ERK activation and ER stress [ 33 ]. ERK1/2 activation can increase Beclin 1 expression and, subsequently, induce autophagy [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

Perfluorooctane sulfonate induces autophagy-associated apoptosis through oxidative stress and the activation of extracellular signal–regulated kinases in renal tubular cells

Chen

Lee

et al. 2021

PLoS ONE

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Perfluorooctane sulfonate (PFOS) is among the most abundant organic pollutants and is widely distributed in the environment, wildlife, and humans. Its toxic effects and biological hazards are associated with its long elimination half-life in humans. However, how it affects renal tubular cells (RTCs) remains unclear. In this study, PFOS was observed to mediate the increase in reactive oxygen species (ROS) generation, followed by the activation of the extracellular-signal-regulated kinase 1/2 (ERK1/2) pathway, which induced autophagy in RTCs. Although PFOS treatment induced autophagy after 6 h, prolonged treatment (24 h) reduced the autophagic flux by increasing lysosomal membrane permeability (LMP), leading to increased p62 protein accumulation and subsequent apoptosis. The increase in LMP was visualized through increased green fluorescence with acridine orange staining, and this was attenuated by 3-methyladenine, an autophagy inhibitor. N-acetyl cysteine and an inhibitor of the mitogen-activated protein kinase kinases (U0126) attenuated autophagy and apoptosis. Taken together, these results indicate that ROS activation and ROS-mediated phosphorylated ERK1/2 activation are essential to activate autophagy, resulting in the apoptosis of PFOS-treated RTCs. Our findings provide insight into the mechanism of PFOS-mediated renal toxicity.

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Section: Discussionmentioning

confidence: 99%

Perfluorooctane sulfonate induces autophagy-associated apoptosis through oxidative stress and the activation of extracellular signal–regulated kinases in renal tubular cells

Chen

Lee

et al. 2021

PLoS ONE

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“…Due to the sensitivity to hypoxia, glucose, and ion disturbance, ER stress is mostly studied in cancer cells [ 14 ]. Reports have documented that ER stress is correlated with cancer cell activation, and an ER chaperone protein, GRP78, is enhanced in cancer cell proliferation and apoptosis through MAPKs, PI3K/Akt, and NF- κ B signalling pathways [ 26 , 27 ]. GRP78 has been postulated as a potential target for cancer cure and a potential prognostic marker [ 14 , 28 ].…”

Section: Discussionmentioning

confidence: 99%

GRP78 Promotes Neural Stem Cell Antiapoptosis and Survival in Response to Oxygen‐Glucose Deprivation (OGD)/Reoxygenation through PI3K/Akt, ERK1/2, and NF‐κB/p65 Pathways

Liu

Zhou

et al. 2018

Oxidative Medicine and Cellular Longevity

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When brain injury happens, endogenous neural stem cells (NSCs) located in the adult subventricular zone (SVZ) and subgranular zone (SGZ) are attacked by ischemia/reperfusion to undergo cellular apoptosis and death before being induced to migrate to the lesion point and differentiate into mature neural cells for damaged cell replacement. Although promoting antiapoptosis and NSC survival are critical to neuroregeneration, the mechanism has yet been elucidated clearly. Here in this study, we established an in vitro oxygen-glucose deprivation (OGD)/reoxygenation model on NSCs and detected glucose-regulated protein 78 (GRP78) involved in apoptosis, while in the absence of GRP78 by siRNA transfection, OGD/reoxygenation triggered PI3K/Akt, ERK1/2, and NF-κB/p65 activation, and induced NSC apoptosis was attenuated. Further investigation, respectively, with the inhibitor of PI3K/Akt or ERK1/2 demonstrated a blockage on GRP78 upregulation, while the inhibition of NF-κB rarely affected GRP78 induction by OGD/reoxygenation. The results indicated the bidirectional regulations of GRP78-PI3K/Akt and GRP78-ERK1/2 and the one-way signalling transduction through GRP78 to NF-κB/p65 on NSC survival from OGD/reoxygenation. In conclusion, we found that GRP78 mediated the signalling cross talk through PI3K/Akt, ERK1/2, and NF-κB/p65, which leads to antiapoptosis and NSC survival from ischemic stroke. Our finding gives a new evidence of GRP78 in NSCs as well as a new piece of signalling mechanism elucidation to NSC survival from ischemic stroke.

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“…Many studies have explored the functional effects of peptides from P. yezoensis , which has exhibited enhanced cell viability by reducing ER stress induced via environmental pollutants [ 28 ]. It also had the ability to decrease oxidative stress caused by hydrogen peroxide and acetaminophen in Chang cells [ 21 , 23 , 24 ].…”

Section: Discussionmentioning

confidence: 99%

Phycoerythrin Peptide from Pyropia yezoensis Alleviates Endoplasmic Reticulum Stress Caused by Perfluorooctane Sulfonate-Induced Calcium Dysregulation

Kim

Nam

2018

Marine Drugs

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Perfluorooctane sulfonate (PFOS), a stable fluorosurfactant, causes endoplasmic reticulum (ER) stress in the brain. This study was designed to investigate whether a phycoerythrin-derived peptide of Pyropia yezoensis (PYP) reduces PFOS-induced ER stress associated with calcium dysregulation. The protective effects of PYP were determined by cell viability, immunoblotting for ER stress response protein glucose-regulated protein 78 (GRP78) and calcium-dependent protein kinases in rat frontal cortical neurons. PFOS-induced decrease in cell viability was attenuated by PYP pretreatment (1 µg/mL) for 24 h, which was downregulated by inhibiting tropomyosin-receptor kinase B (TrkB). PYP pretreatment downregulated the increase in intracellular calcium levels and phosphorylation of calcium/calmodulin-dependent protein kinase II and c-Jun N-terminal kinase which are associated with a PFOS-induced increase in GRP78. The PFOS-induced increase in GRP78 was downregulated via activation of TrkB receptor-linked extracellular signal-regulated kinases 1/2 (ERK1/2) by PYP pretreatment. Moreover, PYP microinjections (1 µg/kg, 0.54 nmol) attenuated the GRP78 expression in rat prefrontal cortex caused by PFOS (10 mg/kg) exposure for 2 weeks. These findings demonstrate that PYP enhances frontal cortical neuron viability via activation of TrkB receptor-ERK1/2 signaling and attenuation of ER stress in rat prefrontal cortex against PFOS exposure, suggesting that PYP might prevent neuronal dysfunctions caused by PFOS-induced ER stress.

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

Cited by 6 publications

References 24 publications

Perfluorooctane sulfonate induces autophagy-associated apoptosis through oxidative stress and the activation of extracellular signal–regulated kinases in renal tubular cells

Perfluorooctane sulfonate induces autophagy-associated apoptosis through oxidative stress and the activation of extracellular signal–regulated kinases in renal tubular cells

GRP78 Promotes Neural Stem Cell Antiapoptosis and Survival in Response to Oxygen‐Glucose Deprivation (OGD)/Reoxygenation through PI3K/Akt, ERK1/2, and NF‐κB/p65 Pathways

Phycoerythrin Peptide from Pyropia yezoensis Alleviates Endoplasmic Reticulum Stress Caused by Perfluorooctane Sulfonate-Induced Calcium Dysregulation

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