The Role of p38 MAPK, JNK, and ERK in Antibacterial Responses of Chilo suppressalis (Lepidoptera: Crambidae)

Qiu, Lin; Zhang, Boyao; Wang, Xiao‐Ping; Lei, Chaoliang; Lin, Yongjun; Zhao, Jing; Ma, Weihua

doi:10.1093/jee/tox126

Cited by 14 publications

(6 citation statements)

References 38 publications

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“…Numerous studies have shown that the MAPKs such as ERK1/2 are activated upon stimulation of cells, including pathogenic infection [40][41][42]. In this context, to further investigate the possible mechanisms underlying the antiinflammation effects of BV, phosphorylation of ERK1/2 was determined in cells exposed to LPS.…”

Section: Discussionmentioning

confidence: 99%

Bee Venom Decreases LPS-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells

Jeong

Cheng

Bae

et al. 2017

Journal of Microbiology and Biotechnology

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The world dairy industry has long been challenged by bovine mastitis, an inflammatory disease, which causes economic loss due to decreased milk production and quality. Attempts have been made to prevent or treat this disease with multiple approaches, primarily through increased abuse of antibiotics, but effective natural solutions remain elusive. Bee venom (BV) contains a variety of peptides (, melittin) and shows multiple bioactivities, including prevention of inflammation. Thus, in the current study, it was hypothesized that BV can reduce inflammation in bovine mammary epithelial cells (MAC-T). To examine the hypothesis, cells were treated with LPS (1 μg/ml) to induce an inflammatory response and the anti-inflammatory effects of BV (2.5 and 5 μg/ml) were investigated. The cellular mechanisms of BV against LPS-induced inflammation were also investigated. Results showed that BV can attenuate expression of an inflammatory protein, COX2, and pro-inflammatory cytokines such as IL-6 and TNF-α. Activation of NF-κB, an inflammatory transcription factor, was significantly downregulated by BV in cells treated with LPS, through dephosphorylation of ERK1/2. Moreover, pretreatment of cells with BV attenuated LPS-induced production of intracellular reactive oxygen species (, superoxide anion). These results support our hypothesis that BV can decrease LPS-induced inflammatory responses in bovine mammary epithelial cells through inhibition of oxidative stress, NF-κB, ERK1/2, and COX-2 signaling.

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Section: Discussionmentioning

confidence: 99%

Bee Venom Decreases LPS-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells

Jeong

Cheng

Bae

et al. 2017

Journal of Microbiology and Biotechnology

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“…In this study, results from both in vivo and in vitro investigations showed that DOX exposure suppressed the nuclear translocation of Nrf2. A set of protein kinases referred as MAPKs were believed to regulate the activation of Nrf2/ARE signaling [ 28 ]. MAPKs including JNK, ERK1/2, and p38MAPK were reported involved in cellular defense responses to stressful factors such as ROS [ 29 ].…”

Section: Discussionmentioning

confidence: 99%

Klotho Improves Cardiac Function by Suppressing Reactive Oxygen Species (ROS) Mediated Apoptosis by Modulating Mapks/Nrf2 Signaling in Doxorubicin-Induced Cardiotoxicity

et al. 2017

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BackgroundAnthracyclines-induced cardiotoxicity has become one of the major restrictions of their clinical applications. Klotho showed cardioprotective effects. This study aimed to investigate the effects and possible mechanisms of klotho on doxorubicin (DOX)-induced cardiotoxicity.Material/MethodsRats and isolated myocytes were exposed to DOX and treated with exogenous klotho. Specific inhibitors and siRNAs silencing MAPKs were also used to treat the animals and/or myocytes. An invasive hemodynamic method was used to determine cardiac functions. Intracellular ROS generation was evaluated by DHE staining. Western blotting was used to determine the phosphorylation levels of JNK, ERK, and p38 MAPKs in plasma extracts and Nrf2 in nuclear extracts. Nuclear translocation of Nrf2 in myocytes was evaluated by immunohistochemistry. Cell apoptosis was evaluated by TUNEL assay and flow cytometry.ResultsKlotho treatment improved DOX-induced cardiac dysfunction in rats. The DOX-induced ROS accumulation and cardiac apoptosis were attenuated by klotho. Impaired phosphorylations of MAPKs, Nrf2 translocation and expression levels of HO1 and Prx1 were also attenuated by klotho treatment. However, the anti-oxidant and anti-apoptotic effects of klotho on DOX-exposed myocardium and myocytes were impaired by both specific inhibitors and siRNAs against MAPKs. Moreover, the recovery effects of klotho on phosphorylations of MAPKs, Nrf2 translocation and expression levels of HO1 and Prx1 were also impaired by specific inhibitors and siRNAs against MAPKs.ConclusionsBy recovering the activation of MAPKs signaling, klotho improved cardiac function loss which was triggered by DOX-induced ROS mediated cardiac apoptosis.

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“…In M. sexta and Aedes aegypti, Cry toxin intoxication activates the p38 MAPK pathway, and the knockdown expression of p38 MAPK leads to an increased sensitivity to Bt Cry toxin (Cancino-Rodezno et al, 2010). Similarly, when the p38 MAPK pathway is silenced via RNAi, the susceptibility of C. suppressalis larvae to the Bt Cry1Ca toxin is significantly increased (Qiu, Fan, et al, 2017). Our results showed that Bt Cry1Ab activated OfERK expression at the transcriptional level at 24, 48, and 72 h posttreatment.…”

Section: The Regulation Of Oferk On Immune- Developmental-and Stress-...mentioning

confidence: 56%

“…It also showed that Cry1Ab toxin significantly induced OfERK expression, and the phylogenetic analysis revealed that OfERK has the closest homolog with Cs‐ERK2 from C. suppressalis . It has been reported that Cs‐ERK 2 is involved in response to Bt infection (Qiu, Zhang, et al, 2017). Therefore, we postulated that OfERK has a potential function in defense against Bt infection.…”

Section: Discussionmentioning

confidence: 99%

Identification and characteristic analysis of an extracellular signal‐regulated kinase from Ostrinia furnacalis Guenée

Li,

Xu,

Zhang

et al. 2023

Arch Insect Biochem Physiol

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The extracellular signal‐regulated kinase (ERK) pathway, a critical genetic determinant, controls diverse physiological functions, including innate immunity, development, and stress response. In the current study, a full‐length cDNA (1592bp) encoding the ERK gene (OfERK) was cloned from Ostrinia furnacalis Guenée (GenBank accession number: MF797866). The open reading frame of the OfERK gene encoded 364 amino acids and shared 96.43%–98.08% amino acid identities with other insect mitogen‐activated protein kinases. For spatiotemporal analysis of the expression pattern, OfERK exhibited a significant peak expression on the 3rd day of the pupa stage and showed the highest expression in hemocytes specifically. Indirect immunofluorescence assays and immuno‐electron microscopy revealed a wide distribution of the OfERK protein in hemocytes and epidermis. Moreover, the results demonstrated that the Bt Cry1Ab‐activated toxin significantly induces the expression of OfERK. Other genes related to immune response, development, and stress response exhibited dynamic changes in expression after Cry1Ab oral treatment. The expression of OfERK was downregulated through RNA interference, and the correlation of its expression with other related genes was verified using quantitative real‐time polymerase chain reaction. Our study provides valuable insights into the regulatory mechanism of ERK in insects for future studies.

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The Role of p38 MAPK, JNK, and ERK in Antibacterial Responses of Chilo suppressalis (Lepidoptera: Crambidae)

Cited by 14 publications

References 38 publications

Bee Venom Decreases LPS-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells

Bee Venom Decreases LPS-Induced Inflammatory Responses in Bovine Mammary Epithelial Cells

Klotho Improves Cardiac Function by Suppressing Reactive Oxygen Species (ROS) Mediated Apoptosis by Modulating Mapks/Nrf2 Signaling in Doxorubicin-Induced Cardiotoxicity

Identification and characteristic analysis of an extracellular signal‐regulated kinase from Ostrinia furnacalis Guenée

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