The Nrf2 molecule trigger antioxidant defense against acute benzo(a)pyrene exposure in the thick shell mussel Mytilus coruscus

Qi, Pengzhi; Tang, Zurong

doi:10.1016/j.aquatox.2020.105554

Cited by 17 publications

(11 citation statements)

References 54 publications

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“…Antioxidants, such as catalase and GR, play an important role in resisting oxidative response and protecting cells. A positive correlation has been found between the expression of Nrf2 and the mRNA level of these antioxidant genes, indicating that Nrf2 is necessary for the long-term induction of these genes [ 58 ]. The demethylation of Keap1 DNA promoter in LECs increases Keapl protein expression, which leads to a decrease in Nrf2 content and the inhibition of antioxidant enzyme gene transcription, thus promoting the occurrence and development of cataract.…”

Section: Discussionmentioning

confidence: 99%

Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function

et al. 2022

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Etiology and pathogenesis of age-related cataract is not entirely clear till now. Senescence marker protein 30 (SMP30) is a newly discovered anti-aging factor, which plays an important role in preventing apoptosis and reducing oxidative stress damage. Mitochondria are located at the intersection of key cellular pathways, such as energy substrate metabolism, reactive oxygen species (ROS) production and apoptosis. Oxidative stress induced by 4-hydroxynonenal (4-HNE) is closely related to neurodegenerative diseases and aging. Our study focused on the effect of SMP30 on mitochondrial homeostasis of human lens epithelial cells (HLECs) induced by 4-HNE. Western blots and qPCR were used to compare the expression of SMP30 protein in the residual lens epithelial cells in the lens capsule of age-related cataract (ARC) patients and the donated transparent lens capsule. On this basis, SMP30 overexpression plasmid and SMP30 shRNA interference plasmid were introduced to explore the effect of SMP30 on the biological behavior in HLECs under the condition of oxidative stress induced by 4-HNE through immunohistochemistry, ROS evaluation, metabolic spectrum analysis and JC-1 fluorescence measurement. Given that Nuclear Factor erythroid 2-Related Factor 2 (Nrf2)/Kelch Like ECH Associated Protein 1 (KEAP1) signaling pathway is the most important antioxidant stress pathway, we further analyzed the regulatory effect of SMP30 by WB to explore its molecular mechanism. Our study indicated that SMP30 may inhibit ROS accumulation, restore mitochondrial function, activate Nrf2/Keap1 signaling pathway, therefore protecting lens epithelial cells from oxidative stress-induced cell damage.

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Section: Discussionmentioning

confidence: 99%

Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function

et al. 2022

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“…A recombinant plasmid termed pET-32a- Mc IL17-1 was generated by subcloning the Mc IL17-1 ORF sequence into the pET-32a prokaryotic expression vector, following transformation into Escherichia coli cells (DE3) (Takara) to express the fusion proteins. The induction and purification of the recombinant protein (r Mc IL17-1) were performed according to our previous report [ 61 ], that the isopropyl-beta-D-thiogalactopy ranoside (IPTG) and Ni-nitorilotriacetic acid (NI-NTA) used as the inducer and depurator, respectively. The purified r Mc IL17-1 was analyzed using SDS-polyacrylamide gel electrophoresis (SDS-PAGE) and visualized with Coomassie brilliant blue R250.…”

Section: Methodsmentioning

confidence: 99%

“…As we described earlier, the RNA interfere assay (RNAi) was performed through the dsRNA injection [ 61 ]. The dsRNA was synthesized by T7 polymerase using Mc IL17-1 cDNA sequence amplified by specific primer pair ( Table 1 , IL17-ds) as the template.…”

Section: Methodsmentioning

confidence: 99%

“…Quantitative real-time PCR (qPCR) was performed on the 7500 Real-Time PCR system (Applied Biosystems, Foster City, CA, USA) with the SYBRR ® premix ExTaq Kit (TaKaRa, Kusatsu, Japan) to assess the transcriptional expression of Mc IL17-1, as previously reported [ 61 ]. The qPCR reaction system was conventional, and the reaction conditions were as follows: 95 °C pre-denaturation for 10 min, 40 cycles of 95 °C denaturation for 10 s and 58 °C annealing for 20 s. Data were analyzed using the 2 –ΔΔCT method with β-actin as an internal reference [ 64 ].…”

Section: Methodsmentioning

confidence: 99%

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An Interleukin-17 Isoform from Thick Shell Mussel Mytilus coruscus Serves as a Mediator of Inflammatory Response

et al. 2023

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The inflammatory cytokine interleukin-17 (IL17) plays an important role in innate immunity by binding to its receptors (IL17Rs) to activate immune defense signals. To date, information on members of the IL17 family is still very limited in molluscan species. Here, a novel member of the IL17 family was identified and characterized from thick shell mussel Mytilus coruscus, and this gene was designated as McIL17-1 by predicting structural domains and phylogenetic analysis. McIL17-1 transcripts existed in all examined tissues with high expression levels in gills, hemocytes and digestive glands. After the stimuli of different pathogen associated molecular patterns (PAMPs) for 72 h, transcriptional expression of McIL17-1 was significantly upregulated, except for poly I:C stimulation. Cytoplasm localization of McIL17-1 was shown in HEK293T cells by fluorescence microscopy. Further, in vivo and in vitro assays were performed to evaluate the potential function of McIL17-1 played in immune response. McIL17-1 was either knocked down or overexpressed in vivo through RNA inference (RNAi) and recombinant protein injection, respectively. With the infection of living Vibrio alginolyticus, a high mortality rate was exhibited in the McIL17-1 overexpressed group compared to the control group, while a lower mortality rate was observed in the McIL17-1 knocked down group than control group. In vitro, the flow cytometric analysis showed that the apoptosis rate of McIL17-1 inhibited hemocytes was significantly lower than that of the control group after lipopolysaccharide stimulation. These results collectively suggested that the newly identified IL17 isoform is involved in the inflammatory response to bacterial infection in M. coruscus.

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“…The Swiss model and pyMol were used to predict the tertiary structure of the Mc IL-17-3 protein. The detailed procedure was according to our previous study [ 66 ].…”

Section: Methodsmentioning

confidence: 99%

Exploring the Role of a Novel Interleukin-17 Homolog from Invertebrate Marine Mussel Mytilus coruscus in Innate Immune Response: Is Negative Regulation by Mc-Novel_miR_145 the Key?

Chen

Qiu

et al. 2023

IJMS

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Interleukin-17 (IL-17) represents a class of proinflammatory cytokines involved in chronic inflammatory and degenerative disorders. Prior to this study, it was predicted that an IL-17 homolog could be targeted by Mc-novel_miR_145 to participate in the immune response of Mytilus coruscus. This study employed a variety of molecular and cell biology research methods to explore the association between Mc-novel_miR_145 and IL-17 homolog and their immunomodulatory effects. The bioinformatics prediction confirmed the affiliation of the IL-17 homolog with the mussel IL-17 family, followed by quantitative real-time PCR assays (qPCR) to demonstrate that McIL-17-3 was highly expressed in immune-associated tissues and responded to bacterial challenges. Results from luciferase reporter assays confirmed the potential of McIL-17-3 to activate downstream NF-κb and its targeting by Mc-novel_miR_145 in HEK293 cells. The study also produced McIL-17-3 antiserum and found that Mc-novel_miR_145 negatively regulates McIL-17-3 via western blotting and qPCR assays. Furthermore, flow cytometry analysis indicated that Mc-novel_miR_145 negatively regulated McIL-17-3 to alleviate LPS-induced apoptosis. Collectively, the current results showed that McIL-17-3 played an important role in molluscan immune defense against bacterial attack. Furthermore, McIL-17-3 was negatively regulated by Mc-novel_miR_145 to participate in LPS-induced apoptosis. Our findings provide new insights into noncoding RNA regulation in invertebrate models.

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The Nrf2 molecule trigger antioxidant defense against acute benzo(a)pyrene exposure in the thick shell mussel Mytilus coruscus

Cited by 17 publications

References 54 publications

Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function

Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function

An Interleukin-17 Isoform from Thick Shell Mussel Mytilus coruscus Serves as a Mediator of Inflammatory Response

Exploring the Role of a Novel Interleukin-17 Homolog from Invertebrate Marine Mussel Mytilus coruscus in Innate Immune Response: Is Negative Regulation by Mc-Novel_miR_145 the Key?

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