C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress
C-phycoerythrin (C-PE) is a phycobiliprotein that prevents oxidative stress and cell damage. The aim of this study was to evaluate whether C-PE also counteracts endoplasmic reticulum (ER) stress as a mechanism contributing to its nephroprotective activity. After C-PE was purified from <i>Phorm...
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2021
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oai:doaj.org-article:e782a3e6855f47119aa53dca02f73ec22021-11-25T18:12:38ZC-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress10.3390/md191105891660-3397https://doaj.org/article/e782a3e6855f47119aa53dca02f73ec22021-10-01T00:00:00Zhttps://www.mdpi.com/1660-3397/19/11/589https://doaj.org/toc/1660-3397C-phycoerythrin (C-PE) is a phycobiliprotein that prevents oxidative stress and cell damage. The aim of this study was to evaluate whether C-PE also counteracts endoplasmic reticulum (ER) stress as a mechanism contributing to its nephroprotective activity. After C-PE was purified from <i>Phormidium persicinum</i> by using size exclusion chromatography, it was characterized by spectrometry and fluorometry. A mouse model of HgCl<sub>2</sub>-induced acute kidney injury (AKI) was used to assess the effect of C-PE treatment (at 25, 50, or 100 mg/kg of body weight) on oxidative stress, the redox environment, and renal damage. ER stress was examined with the same model and C-PE treatment at 100 mg/kg. C-PE diminished oxidative stress and cell damage in a dose-dependent manner by impeding the decrease in expression of nephrin and podocin normally caused by mercury intoxication. It reduced ER stress by preventing the activation of the inositol-requiring enzyme-1α (IRE1α) pathway and avoiding caspase-mediated cell death, while leaving the expression of protein kinase RNA-like ER kinase (PERK) and activating transcription factor 6α (ATF6α) pathways unmodified. Hence, C-PE exhibited a nephroprotective effect on HgCl<sub>2</sub>-induced AKI by reducing oxidative stress and ER stress.Vanessa Blas-ValdiviaPlácido Rojas-FrancoJose Ivan Serrano-ContrerasAndrea Augusto SfrisoCristian Garcia-HernandezMargarita Franco-ColínEdgar Cano-EuropaMDPI AGarticleC-phycoerythrin<i>Phormidium persicinum</i>acute kidney injurymercuryoxidative stressendoplasmic reticulum stressBiology (General)QH301-705.5ENMarine Drugs, Vol 19, Iss 589, p 589 (2021) |
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C-phycoerythrin <i>Phormidium persicinum</i> acute kidney injury mercury oxidative stress endoplasmic reticulum stress Biology (General) QH301-705.5 |
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C-phycoerythrin <i>Phormidium persicinum</i> acute kidney injury mercury oxidative stress endoplasmic reticulum stress Biology (General) QH301-705.5 Vanessa Blas-Valdivia Plácido Rojas-Franco Jose Ivan Serrano-Contreras Andrea Augusto Sfriso Cristian Garcia-Hernandez Margarita Franco-Colín Edgar Cano-Europa C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress |
description |
C-phycoerythrin (C-PE) is a phycobiliprotein that prevents oxidative stress and cell damage. The aim of this study was to evaluate whether C-PE also counteracts endoplasmic reticulum (ER) stress as a mechanism contributing to its nephroprotective activity. After C-PE was purified from <i>Phormidium persicinum</i> by using size exclusion chromatography, it was characterized by spectrometry and fluorometry. A mouse model of HgCl<sub>2</sub>-induced acute kidney injury (AKI) was used to assess the effect of C-PE treatment (at 25, 50, or 100 mg/kg of body weight) on oxidative stress, the redox environment, and renal damage. ER stress was examined with the same model and C-PE treatment at 100 mg/kg. C-PE diminished oxidative stress and cell damage in a dose-dependent manner by impeding the decrease in expression of nephrin and podocin normally caused by mercury intoxication. It reduced ER stress by preventing the activation of the inositol-requiring enzyme-1α (IRE1α) pathway and avoiding caspase-mediated cell death, while leaving the expression of protein kinase RNA-like ER kinase (PERK) and activating transcription factor 6α (ATF6α) pathways unmodified. Hence, C-PE exhibited a nephroprotective effect on HgCl<sub>2</sub>-induced AKI by reducing oxidative stress and ER stress. |
format |
article |
author |
Vanessa Blas-Valdivia Plácido Rojas-Franco Jose Ivan Serrano-Contreras Andrea Augusto Sfriso Cristian Garcia-Hernandez Margarita Franco-Colín Edgar Cano-Europa |
author_facet |
Vanessa Blas-Valdivia Plácido Rojas-Franco Jose Ivan Serrano-Contreras Andrea Augusto Sfriso Cristian Garcia-Hernandez Margarita Franco-Colín Edgar Cano-Europa |
author_sort |
Vanessa Blas-Valdivia |
title |
C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress |
title_short |
C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress |
title_full |
C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress |
title_fullStr |
C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress |
title_full_unstemmed |
C-phycoerythrin from <i>Phormidium persicinum</i> Prevents Acute Kidney Injury by Attenuating Oxidative and Endoplasmic Reticulum Stress |
title_sort |
c-phycoerythrin from <i>phormidium persicinum</i> prevents acute kidney injury by attenuating oxidative and endoplasmic reticulum stress |
publisher |
MDPI AG |
publishDate |
2021 |
url |
https://doaj.org/article/e782a3e6855f47119aa53dca02f73ec2 |
work_keys_str_mv |
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