Elevated ER stress exacerbates dextran sulfate sodium-induced colitis in PRDX4-knockout mice

Takagi, Tomohisa; Homma, Takujiro; Fujii, Junichi; Shirasawa, Nobuyuki; Yoriki, Hiroyuki; Hotta, Yuma; Higashimura, Yasuki; Mizushima, Katsura; Hirai, Yasuko; Katada, Kazuhiro; Uchiyama, Kazuhiko; Naito, Yuji; Itoh, Yoshito

doi:10.1016/j.freeradbiomed.2018.12.024

Cited by 21 publications

(22 citation statements)

References 48 publications

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“…Additionally, Prdx4 deficiency leads to increases in misfolded proteins and H 2 O 2 in the ER lumen, inducing ER stress 39 . Furthermore, studies have demonstrated that when using a dextran sulphate sodium (DSS)-induced colitis model, lack of Prdx4 aggravates the colonic mucosal damage caused by ER stress 40 . Prdx4 functions as an ER thiol oxidase and antioxidant and protects the homeostasis of the cell environment.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 4 protects against ovarian ageing by ameliorating d-galactose-induced oxidative damage in mice

Liang

Yan

et al. 2020

Cell Death Dis

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Peroxiredoxin 4 (Prdx4), a member of the Prdx family, is a vital ER-resident antioxidant in cells. As revealed in our previous study, Prdx4 expression was detected in ovarian granulosa cells and was closely related to ovarian function. This research aimed to explore the effect and underlying molecular mechanism of the protective role of Prdx4 against d-gal-induced ovarian ageing in mice. The d-gal-induced ovarian ageing model has been extensively used to study the mechanisms of premature ovarian failure (POF). In this study, adult Prdx4−/− and wild-type mice were intraperitoneally injected with d-gal (150 mg/kg/day) daily for 6 weeks. Ovarian function, granulosa cell apoptosis, oxidative damage and ER stress in the ovaries were evaluated in the two groups. Ovarian weight was significantly lower, the HPO axis was more strongly disrupted, and the numbers of atretic follicles and apoptotic granulosa cells were obviously higher in Prdx4−/− mice. In addition, Prdx4−/− mice showed increased expression of oxidative damage-related factors and the ovarian senescence-related protein P16. Moreover, the levels of the proapoptotic factors CHOP and activated caspase-12 protein, which are involved in the ER stress pathway, and the level of the apoptosis-related BAX protein were elevated in the ovaries of Prdx4−/− mice. Thus, d-gal-induced ovarian ageing is accelerated in Prdx4−/− mice due to granulosa cell apoptosis via oxidative damage and ER stress-related pathways, suggesting that Prdx4 is a protective agent against POF.

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Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 4 protects against ovarian ageing by ameliorating d-galactose-induced oxidative damage in mice

Liang

Yan

et al. 2020

Cell Death Dis

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“…PRDX4 is an antioxidant enzyme located in the endoplasmic reticulum (ER) and plays an important role in H 2 O 2 scavenging and protein folding in the ER [57]. PRDX4 deficiency has been found to exacerbate diethylnitrosamine-induced hepatic oxidative stress [58] and dextran sulfate sodium-induced intestinal inflammation [59]. Thus, the reduction of PRDX4 expression might be an important contributor for the elevated oxidative stress in PM 2.5 -3H-exposed lungs.…”

Section: Discussionmentioning

confidence: 99%

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

et al. 2019

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The association between airborne fine particulate matter (PM 2.5 ) concentration and the risk of respiratory diseases has been well documented by epidemiological studies. However, the mechanism underlying the harmful effect of PM 2.5 has not been fully understood. In this study, we exposed the C57BL/6J mice to airborne PM 2.5 for 3 months (mean daily concentration ~50 or ~110 μg/m 3 , defined as PM 2.5 –3L or PM 2.5 –3H) or 6 months (mean daily concentration ~50 μg/m 3 , defined as PM 2.5 –6L) through a whole-body exposure system. Histological and biochemical analysis revealed that PM 2.5 –3H exposure caused more severe lung injury than did PM 2.5 –3L, and the difference was greater than that of PM 2.5 –6L vs PM 2.5 –3L exposure. With RNA-sequencing technique, we found that the lungs exposed with different concentration of PM 2.5 have distinct transcriptional profiles. PM 2.5 –3H exposure caused more differentially expressed genes (DEGs) in lungs than did PM 2.5 –3L or PM 2.5 –6L. The DEGs induced by PM 2.5 –3L or PM 2.5 –6L exposure were mainly enriched in immune pathways, including Hematopoietic cell lineage and Cytokine-cytokine receptor interaction, while the DEGs induced by PM 2.5 –3H exposure were mainly enriched in cardiovascular disease pathways, including Hypertrophic cardiomyopathy and Dilated cardiomyopathy. In addition, we found that upregulation of Cd5l and reduction of Hspa1 and peroxiredoxin-4 was associated with PM 2.5 -induced pulmonary inflammation and oxidative stress. These results may provide new insight into the cytotoxicity mechanism of PM 2.5 and help to development of new strategies to attenuate air pollution associated respiratory disease.

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“…Spermatogenic cells in Prdx4 −/y are susceptible to cell death by oxidative stress [89]. In a DSS-induced colitis model, Prdx4 −/y show loss of body weight and shortening of colon length, which may be caused by ER stress and oxidative damage in colonic epithelial cells [90]. Prdx4 −/y show a higher incidence of hepatocellular carcinoma in the diethylnitrosamine injection model compared with that of wild-type mice [91].…”

Section: Phenotypesmentioning

confidence: 99%

Knockout Mouse Models for Peroxiredoxins

Lee

2020

Antioxidants

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Peroxiredoxins (PRDXs) are members of a highly conserved peroxidase family and maintain intracellular reactive oxygen species (ROS) homeostasis. The family members are expressed in most organisms and involved in various biological processes, such as cellular protection against ROS, inflammation, carcinogenesis, atherosclerosis, heart diseases, and metabolism. In mammals, six PRDX members have been identified and are subdivided into three subfamilies: typical 2-Cys (PRDX1, PRDX2, PRDX3, and PRDX4), atypical 2-Cys (PRDX5), and 1-Cys (PRDX6) subfamilies. Knockout mouse models of PRDXs have been developed to investigate their in vivo roles. This review presents an overview of the knockout mouse models of PRDXs with emphases on the biological and physiological changes of these model mice.

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Elevated ER stress exacerbates dextran sulfate sodium-induced colitis in PRDX4-knockout mice

Cited by 21 publications

References 48 publications

Peroxiredoxin 4 protects against ovarian ageing by ameliorating d-galactose-induced oxidative damage in mice

Peroxiredoxin 4 protects against ovarian ageing by ameliorating d-galactose-induced oxidative damage in mice

The effect of exposure time and concentration of airborne PM2.5 on lung injury in mice: A transcriptome analysis

Knockout Mouse Models for Peroxiredoxins

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