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Oxidative Stress-mediated Sprouty-related Protein with an EVH1 Domain 1 Down-regulation Contributes to Resisting Oxidative Injury in Microglia

Wei, Li, Li, Xin, Wei, Qianfeng, Chen, Lin, Xu, Li, Zhou, Peng·2023·Neuroscience
DOI 10.1016/j.neuroscience.2023.06.012
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Fig. 1 ( A ) TTC-stained mice brain slice after experimental stroke (MCAO, 60 min occlusion, 24 h reperfusion). ( B ) The expression levels of eNOS, iNOS, SOD1, SOD2 after MCAO treatment in cerebral cortex. GAPDH was used as a loading control. ( C ) Quantification of the malondialdehyde (MDA) in cerebral cortex after MCAO treatment. ( D, E ) The activities of superoxide dismutase (SOD) and catalase were detected in cerebral cortex after MCAO treatment. (*, p < 0.05, n = 5) ( F ) The representative images of immune-histochemical assays for SPRED1 expression in cerebral cortex. ( G ) The expression levels of SPRED1 after MCAO treatment in cerebral cortex. GAPDH was used as a loading control. ( H ) Quantification of the SPRED1 protein level after MCAO treatment. (*, p <0.05).
Fig. 1 ( A ) TTC-stained mice brain slice after experimental stroke (MCAO, 60 min occlusion, 24 h reperfusion). ( B ) The expression levels of eNOS, iNOS, SOD1, SOD2 after MCAO treatment in cerebral cortex. GAPDH was used as a loading control. ( C ) Quantification of the malondialdehyde (MDA) in cerebral cortex after MCAO treatment. ( D, E ) The activities of superoxide dismutase (SOD) and catalase were detected in cerebral cortex after MCAO treatment. (*, p < 0.05, n = 5) ( F ) The representative images of immune-histochemical assays for SPRED1 expression in cerebral cortex. ( G ) The expression levels of SPRED1 after MCAO treatment in cerebral cortex. GAPDH was used as a loading control. ( H ) Quantification of the SPRED1 protein level after MCAO treatment. (*, p <0.05).CC-BY-NC-ND · From the PDF
Fig. 2 ( A ) Schematic representation of the domains of SPRED1 of human origin. ( B, C ) Detection of the level of SPRED1 protein in BV2 cells after 100 l M H2O2 treatment for 1, 3, 6, 12 and 24 h, and quantified in the right (C). GAPDH was used as a loading control. ( D-F ) Detection of the levels of p38, p65, SOD1 and SOD2 proteins in BV2 cells after 100 l M H2O2 treatment for 1, 3, 6, 12 and 24 h, quantified in the right (E) and below (F). b -actin was used as a loading control.
Fig. 2 ( A ) Schematic representation of the domains of SPRED1 of human origin. ( B, C ) Detection of the level of SPRED1 protein in BV2 cells after 100 l M H2O2 treatment for 1, 3, 6, 12 and 24 h, and quantified in the right (C). GAPDH was used as a loading control. ( D-F ) Detection of the levels of p38, p65, SOD1 and SOD2 proteins in BV2 cells after 100 l M H2O2 treatment for 1, 3, 6, 12 and 24 h, quantified in the right (E) and below (F). b -actin was used as a loading control.CC-BY-NC-ND · From the PDF
Fig. 3 ( A, B ) Detection of the levels of SPRED1, p38 and p65 proteins in BV2 cells after transfected by SPRED1 plasmid along with the treatment of H2O2, and quantified their levels in ( B ). GAPDH was used as the loading control. ( C, D ) Detect the levels of TNFa and IL-1 b via ELISA kits in BV2 cells after treatment as the procedures in ( A, B ) for 24 h. (*, p <0.05).
Fig. 3 ( A, B ) Detection of the levels of SPRED1, p38 and p65 proteins in BV2 cells after transfected by SPRED1 plasmid along with the treatment of H2O2, and quantified their levels in ( B ). GAPDH was used as the loading control. ( C, D ) Detect the levels of TNFa and IL-1 b via ELISA kits in BV2 cells after treatment as the procedures in ( A, B ) for 24 h. (*, p <0.05).CC-BY-NC-ND · From the PDF
Fig. 4 ( A ) The relative value of CCK-8 in BV2 cells after transfection with H2O2 or/and pcDNA3.1-SPRED1 for 24 h. ( B ) Flow cytometer was used to detect the fluorescence intensity of PI-labeled and FITC-labeled after transfection. ( C ) According to streaming results, the average fluorescence intensity of each group was counted. ( D, E ) Detection of the levels of Bax and Bcl2 proteins in BV2 cells after transfection, quantified in the right (E). GAPDH was used as a loading control. (*, p <0.05).
Fig. 4 ( A ) The relative value of CCK-8 in BV2 cells after transfection with H2O2 or/and pcDNA3.1-SPRED1 for 24 h. ( B ) Flow cytometer was used to detect the fluorescence intensity of PI-labeled and FITC-labeled after transfection. ( C ) According to streaming results, the average fluorescence intensity of each group was counted. ( D, E ) Detection of the levels of Bax and Bcl2 proteins in BV2 cells after transfection, quantified in the right (E). GAPDH was used as a loading control. (*, p <0.05).CC-BY-NC-ND · From the PDF

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Research works printed but not linked: 25

  1. Ablain, 2018, Human tumor genomics and zebrafish modeling identify SPRED1 loss as a driver of mucosal melanoma, Science, 362, 1055, 10.1126/science.aau6509 · DOI
  2. Barone, 2001, Inhibition of p38 mitogen-activated protein kinase provides neuroprotection in cerebral focal ischemia, Med Res Rev, 21, 129, 10.1002/1098-1128(200103)21:2<129::AID-MED1003>3.0.CO;2-H · DOI
  3. Chen, 2011, Oxidative stress in ischemic brain damage: Mechanisms of cell death and potential molecular targets for neuroprotection, Antioxid Redox Sign, 14, 1505, 10.1089/ars.2010.3576 · DOI
  4. Chen, 2020, Therapeutic targets of oxidative/nitrosative stress and neuroinflammation in ischemic stroke: Applications for natural product efficacy with omics and systemic biology, Pharmacol Res, 158, 10.1016/j.phrs.2020.104877 · DOI
  5. Dunzendorfer-Matt, 2016, The neurofibromin recruitment factor Spred1 binds to the GAP related domain without affecting Ras inactivation, Proc Natl Acad Sci USA, 113, 7497, 10.1073/pnas.1607298113 · DOI
  6. Ferrer, 2003, Early modifications in the expression of mitogen-activated protein kinase (MAPK/ERK), stress-activated kinases SAPK/JNK and p38, and their phosphorylated substrates following focal cerebral ischemia, Acta Neuropathol, 105, 425, 10.1007/s00401-002-0661-2 · DOI
  7. Gallo, 2002, Mixed-lineage kinase control of JNK and p38 MAPK pathways, Nat Rev Mol Cell Bio, 3, 663, 10.1038/nrm906 · DOI
  8. He, 2020, Highly bioactive zeolitic imidazolate framework-8-capped nanotherapeutics for efficient reversal of reperfusion-induced injury in ischemic stroke, Sci Adv, 6, 10.1126/sciadv.aay9751 · DOI
  9. Hu, 2015, miR-126 promotes angiogenesis and attenuates inflammation after contusion spinal cord injury in rats, Brain Res, 1608, 191, 10.1016/j.brainres.2015.02.036 · DOI
  10. Li, 2016, Neuron-derived FGF10 ameliorates cerebral ischemia injury via inhibiting NF-kappa B-dependent neuroinflammation and activating PI3K/Akt survival signaling pathway in mice, Sci Rep-Uk, 6
  11. Liang, 2019, Preactivation of Notch1 in remote ischemic preconditioning reduces cerebral ischemia-reperfusion injury through crosstalk with the NF-kappa B pathway, J Neuroinflamm, 16, 10.1186/s12974-019-1570-9 · DOI
  12. Park, 2018, RPM-1 and DLK-1 regulate pioneer axon outgrowth by controlling Wnt signaling, Development, 145, 10.1242/dev.164897 · DOI
  13. Phoenix, 2010, Spred1, a negative regulator of Ras-MAPK-ERK, is enriched in CNS germinal zones, dampens NSC proliferation, and maintains ventricular zone structure, Gene Dev, 24, 45, 10.1101/gad.1839510 · DOI
  14. Ridder, 2009, NF-kappa B signaling in cerebral ischemia, Neuroscience, 158, 995, 10.1016/j.neuroscience.2008.07.007 · DOI
  15. Sanderson, 2013, Molecular mechanisms of ischemia-reperfusion injury in brain: Pivotal role of the mitochondrial membrane potential in reactive oxygen species generation, Mol Neurobiol, 47, 9, 10.1007/s12035-012-8344-z · DOI
  16. Sun, 2017, Dyrk2 involved in regulating LPS-induced neuronal apoptosis, Int J Biol Macromol, 104, 979, 10.1016/j.ijbiomac.2017.06.087 · DOI
  17. Sun, 2022, High-performance SOD mimetic enzyme Au@Ce for arresting cell cycle and proliferation of acute myeloid leukemia, Bioact Mater, 10, 117
  18. Sun, 2022, Coronal relay reactor Fe3O4@CeO2 for accelerating ROS axial conversion through enhanced Enzyme-like effect and relay effect, Chem Eng J, 429, 10.1016/j.cej.2021.132303 · DOI
  19. Tadokoro, 2018, Spred1 safeguards hematopoietic homeostasis against diet-induced systemic stress, Cell Stem Cell, 22, 713, 10.1016/j.stem.2018.04.002 · DOI
  20. Wakioka, 2001, Spred is a Sprouty-related suppressor of Ras signalling, Nature, 412, 647, 10.1038/35088082 · DOI
  21. Xu, 2018, Dyrk2 mediated the release of proinflammatory cytokines in LPS-induced BV2 cells, Int J Biol Macromol, 109, 1115, 10.1016/j.ijbiomac.2017.11.095 · DOI
  22. Yan, 2020, Structural insights into the SPRED1-neurofibromin-KRAS complex and disruption of SPRED1-neurofibromin interaction by oncogenic EGFR, Cell Rep, 32, 10.1016/j.celrep.2020.107909 · DOI
  23. Yang, 2018, Diverse roles of mitochondria in ischemic stroke, Redox Biol, 16, 263, 10.1016/j.redox.2018.03.002 · DOI
  24. Yang, 2020, Neuroprotective and anti-inflammatory effect of tangeretin against cerebral ischemia-reperfusion injury in rats, Inflammation, 43, 2332, 10.1007/s10753-020-01303-z · DOI
  25. Zhao, 2017, Regulation of microglial activation in stroke, Acta Pharmacol Sin, 38, 445, 10.1038/aps.2016.162 · DOI

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Metadata

Authors
Wei, L., Li, X., Wei, Q., Chen, L., Xu, L., & Zhou, P.
Venue
Neuroscience
Publisher
Elsevier BV
Published
2023-08
Volume
526
Pages
13-20
ISSN
0306-4522
DOI
10.1016/j.neuroscience.2023.06.012
Cited by
3
References
1
Language
en
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CoChat. (2026). Citation check: Oxidative Stress-mediated Sprouty-related Protein with an EVH1 Domain 1 Down-regulation Contributes to Resisting Oxidative Injury in Microglia. https://app.cochat.ai/papers/10.1016/j.neuroscience.2023.06.012
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Wei, L., Li, X., Wei, Q., Chen, L., Xu, L., & Zhou, P. (2023). Oxidative Stress-mediated Sprouty-related Protein with an EVH1 Domain 1 Down-regulation Contributes to Resisting Oxidative Injury in Microglia. Neuroscience. https://doi.org/10.1016/j.neuroscience.2023.06.012