Prdx1 alleviates cardiomyocyte apoptosis through ROS-activated MAPK pathway during myocardial ischemia/reperfusion injury

Guo, Wanwan; Liu, Xiaojuan; Li, Jingjing; Shen, Yimin; Zhou, Zijian; Wang, Mingming; Xie, Yuyi; Feng, Xiao; Wang, Liyang; Xiang, Wu

doi:10.1016/j.ijbiomac.2018.02.009

Cited by 67 publications

(50 citation statements)

References 37 publications

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“…15 During myocardial ischemia/reperfusion damage, PRDX1 can also reduce myocardial apoptosis through the reactive oxygen species-activated mitogen-activated protein kinase pathway. 16 According to autophagy studies, PRDX1 can negatively regulate the signaling and autophagy functions of toll-like receptor 4 activated by nuclear factor-κB by inhibiting the activity of tumor necrosis factor receptor-associated factor 6 ubiquitinligase. Moreover, it can enhance bactericidal activity and inhibit the invasion and migration of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

<p>Silencing of Peroxiredoxin 1 Inhibits the Proliferation of Esophageal Cancer Cells and Promotes Apoptosis by Inhibiting the Activity of the PI3K/AKT Pathway</p>

Song¹,

Liu²,

Cui³

et al. 2019

CMAR

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Objective: To study the effect of peroxiredoxin 1 (PRDX1) on esophageal squamous carcinoma cells and determine whether it plays a role in regulating the PI3K/AKT signaling pathway. Methods: Three esophageal squamous cell carcinoma cell lines (Eca-109, EC9706, and KYSE150) and one normal cell line (human esophageal epithelial cells) were selected. The protein expression of peroxiredoxin 1 (PRDX1) and the activity of the PI3K/AKT pathway were detected via Western blotting. The proliferation ability of cells was detected through the MTT assay and cell clone formation. Apoptosis was detected using flow cytometry. Subsequently, cells were treated with a PI3K/AKT pathway inhibitor and activator, alone or in combination with silencing of PRDX1, and the above indicators were re-tested. Results: The expression of PRDX1 and activity of PI3K/AKT pathway-associated proteins were higher in esophageal cancer cells than in normal esophageal epithelial cells. Compared with normal human esophageal epithelial cells, the proliferation of the three types of esophageal cancer cells was increased, whereas their level of apoptosis was decreased (p<0.05). In Eca-109 cells (cell line with silenced expression of PRDX1), the expression of PRDX1 was significantly decreased. In contrast to the control group, the proliferation and clonality of cells in the silencing PRDX1 group was decreased, the proportion of apoptotic cells was increased, and the phosphorylation levels of PI3K and AKT were decreased (p<0.05). Compared with the control group, treatment with the inhibitor LY294002 alone significantly inhibited cell proliferation and promoted apoptosis (p<0.05); this effect was similar to that observed in the silencing PRDX1 group. Conclusion: PRDX1 was highly expressed in esophageal cancer cells. Silencing of PRDX1 can inhibit the proliferation of esophageal cancer cells and promote apoptosis. The mechanism involved in this process may be related to the inhibition of the PI3K/AKT signaling pathway.

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Section: Discussionmentioning

confidence: 99%

<p>Silencing of Peroxiredoxin 1 Inhibits the Proliferation of Esophageal Cancer Cells and Promotes Apoptosis by Inhibiting the Activity of the PI3K/AKT Pathway</p>

Song¹,

Liu²,

Cui³

et al. 2019

CMAR

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“…Cells were washed and subjected to flow cytometric analysis. e excitation wavelength was 488 nm and the observation wavelength was 525 nm for green fluorescence [26].…”

Section: Analysis Of Ros Productionmentioning

confidence: 99%

PCK1Deficiency Shortens the Replicative Lifespan ofSaccharomyces cerevisiaethrough Upregulation ofPFK1

Yuan

Lin

Cui

et al. 2020

BioMed Research International

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The cytosolic isozyme of phosphoenolpyruvate carboxykinase (PCK1) was the first rate-limiting enzyme in the gluconeogenesis pathway, which exerted a critical role in maintaining the blood glucose levels. PCK1 has been established to be involved in various physiological and pathological processes, including glucose metabolism, lipid metabolism, diabetes, and tumorigenesis. Nonetheless, the association of PCK1 with aging process and the detailed underlying mechanisms of PCK1 on aging are still far to be elucidated. Hence, we herein constructed the PCK1-deficient (pck1Δ) and PCK1 overexpression (PCK1 OE) Saccharomyces cerevisiae. The results unveiled that PCK1 deficiency significantly shortened the replicative lifespan (RLS) in the S. cerevisiae, while overexpression of PCK1 prolonged the RLS. Additionally, we noted that the ROS level was significantly enhanced in PCK1-deficient strain and decreased in PCK1 OE strain. Then, a high throughput analysis by deep sequencing was performed in the pck1Δ and wild-type strains, in an attempt to shed light on the effect of PCK1 on the lifespan of aging process. The data showed that the most downregulated mRNAs were enriched in the regulatory pathways of glucose metabolism. Fascinatingly, among the differentially expressed mRNAs, PFK1 was one of the most upregulated genes, which was involved in the glycolysis process and ROS generation. Thus, we further constructed the pfk1Δpck1Δ strain by deletion of PFK1 in the PCK1-deficient strain. The results unraveled that pfk1Δpck1Δ strain significantly suppressed the ROS level and restored the RLS of pck1Δ strain. Taken together, our data suggested that PCK1 deficiency enhanced the ROS level and shortened the RLS of S. cerevisiae via PFK1.

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“…Previous studies on the molecular regulatory mechanism of MIRI mainly focus on the signaling pathways relevant to cell growth and survival, such as the mitogenactivated protein kinase (MAPK) signal transduction pathway [7] and the phosphatidylinositol 3-hydroxy kinase/protein kinase B/, PI3K/Akt signal transduction pathway [8]. ERK, JNK, and p38 are the 3 most important MAPK signaling pathways, which are also the most related approaches in the search for potential targeted drugs for the treatment of AMI [9].…”

Section: Introductionmentioning

confidence: 99%

Paeoniflorin on Rat Myocardial Ischemia Reperfusion Injury of Protection and Mechanism Research

et al. 2019

Pharmacology

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Objective: To study the myocardial benefit effect and mechanism of paeoniflorin on myocardial ischemia reperfusion injury (MIRI) in rats. Methods: Hundred SD rats were randomly divided into 5 groups: sham group, model group, Paeoniflorin (15 mg/kg) group, Paeoniflorin (30 mg/kg) group, and Paeoniflorin (60 mg/kg) group. Myocardial ischemia reperfusion model was established in each group except the sham group. The myocardial infarction and morphological changes were measured by the TTC staining and HE staining respectively. Myocardial caspase-3 was detected by immunohistochemistry. In addition, the protein levels of Bcl-2 and Bax and the expression ratio of p-erk, p-jnk, and p-p38 were detected by Western blot. Myocardial superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were measured by the assay kit. Results: Paeoniflorin (30 mg/kg) and Paeoniflorin (60 mg/kg) can obviously alleviate myocardial infarction caused by MIRI (p < 0.05). HE staining showed that the myocardial morphology in the treatment group was obviously better than that in the model group. WB and immunohistochemistry showed that Paeoniflorin (30 mg/kg) andPaeoniflorin (60 mg/kg) can significantly increase the reduced protein level of bcl-2 (p < 0.05) and reduce the increased protein level of caspase3, bax p-erk, p-jnk, and p-p38 caused by MIRI (p < 0.05). The activity of SOD was increased and the level of MDA was decreased after Paeoniflorin treatment. Conclusion: Paeoniflorin preconditioning has a protective effect on MIRI in rats. Its mechanism is related to reducing oxidative stress and apoptosis by inhibiting the expression of apoptosis-related signaling pathway.

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Prdx1 alleviates cardiomyocyte apoptosis through ROS-activated MAPK pathway during myocardial ischemia/reperfusion injury

Cited by 67 publications

References 37 publications

<p>Silencing of Peroxiredoxin 1 Inhibits the Proliferation of Esophageal Cancer Cells and Promotes Apoptosis by Inhibiting the Activity of the PI3K/AKT Pathway</p>

<p>Silencing of Peroxiredoxin 1 Inhibits the Proliferation of Esophageal Cancer Cells and Promotes Apoptosis by Inhibiting the Activity of the PI3K/AKT Pathway</p>

PCK1Deficiency Shortens the Replicative Lifespan ofSaccharomyces cerevisiaethrough Upregulation ofPFK1

Paeoniflorin on Rat Myocardial Ischemia Reperfusion Injury of Protection and Mechanism Research

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