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    Alomone Labs wrw4
    PSMα1-induced neutrophil necroptosis was blocked by <t>WRW4</t> or anti-TNFα. a, c Neutrophil were treated with PBS or TNFα neutralizing antibody at indicated concentrations for 1 h prior to the incubation with 1 μM PSMα1 for 1 h. The release of LDH was detected ( n = 6) and the level of pMLKL, MLKL and β-actin in neutrophil were detected by western blot ( n = 3). b, d, e Neutrophil were treated with PBS or WRW4 at indicated concentrations for 1 h prior to the incubation with 1 μM PSMα1 for 1 h. The release of LDH was detected ( n = 6), the level of pMLKL, MLKL and β-actin in neutrophil were detected by western blot ( n = 3), and the level of TNFα was detected by ELISA assay ( n = 8). Data were shown as mean ± SE (a, b, e). * P
    Wrw4, supplied by Alomone Labs, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    PSMα1-induced neutrophil necroptosis was blocked by WRW4 or anti-TNFα. a, c Neutrophil were treated with PBS or TNFα neutralizing antibody at indicated concentrations for 1 h prior to the incubation with 1 μM PSMα1 for 1 h. The release of LDH was detected ( n = 6) and the level of pMLKL, MLKL and β-actin in neutrophil were detected by western blot ( n = 3). b, d, e Neutrophil were treated with PBS or WRW4 at indicated concentrations for 1 h prior to the incubation with 1 μM PSMα1 for 1 h. The release of LDH was detected ( n = 6), the level of pMLKL, MLKL and β-actin in neutrophil were detected by western blot ( n = 3), and the level of TNFα was detected by ELISA assay ( n = 8). Data were shown as mean ± SE (a, b, e). * P

    Journal: Cell Death & Disease

    Article Title: Inhibiting PSMα-induced neutrophil necroptosis protects mice with MRSA pneumonia by blocking the agr system

    doi: 10.1038/s41419-018-0398-z

    Figure Lengend Snippet: PSMα1-induced neutrophil necroptosis was blocked by WRW4 or anti-TNFα. a, c Neutrophil were treated with PBS or TNFα neutralizing antibody at indicated concentrations for 1 h prior to the incubation with 1 μM PSMα1 for 1 h. The release of LDH was detected ( n = 6) and the level of pMLKL, MLKL and β-actin in neutrophil were detected by western blot ( n = 3). b, d, e Neutrophil were treated with PBS or WRW4 at indicated concentrations for 1 h prior to the incubation with 1 μM PSMα1 for 1 h. The release of LDH was detected ( n = 6), the level of pMLKL, MLKL and β-actin in neutrophil were detected by western blot ( n = 3), and the level of TNFα was detected by ELISA assay ( n = 8). Data were shown as mean ± SE (a, b, e). * P

    Article Snippet: WRW4 (Alomone Labs, USA) is an antagonist of FPR2.

    Techniques: Incubation, Western Blot, Enzyme-linked Immunosorbent Assay

    Schematic illustration of the targets of beneficial MR-39 action in LPS-stimulated microglial cells. The varied action of MR-39 in microglia cells includes reduction of the lactate dehydrogenase release, inhibition of the caspase-3 activity, and reactive oxide production as well as nitric oxide release evoked by bacterial endotoxin treatment. Moreover, MR-39 exerts an anti-inflammatory effect related to the inhibition of the synthesis of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6). This action is mediated by the reduction of ERK1/2 and the NF-κB transcription factor phosphorylation. Abbreviations: FPR2: formyl peptide receptor2; LDH: lactate dehydrogenase; LPS: lipopolysaccharide; ERK1/2: extracellular signal-regulated kinases; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; ROS: reactive oxygen species; NO: nitric oxide; TNF-α: tumor necrosis factor α; IL-1β: interleukin 1β; IL-6: interleukin 6.

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: Schematic illustration of the targets of beneficial MR-39 action in LPS-stimulated microglial cells. The varied action of MR-39 in microglia cells includes reduction of the lactate dehydrogenase release, inhibition of the caspase-3 activity, and reactive oxide production as well as nitric oxide release evoked by bacterial endotoxin treatment. Moreover, MR-39 exerts an anti-inflammatory effect related to the inhibition of the synthesis of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6). This action is mediated by the reduction of ERK1/2 and the NF-κB transcription factor phosphorylation. Abbreviations: FPR2: formyl peptide receptor2; LDH: lactate dehydrogenase; LPS: lipopolysaccharide; ERK1/2: extracellular signal-regulated kinases; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; ROS: reactive oxygen species; NO: nitric oxide; TNF-α: tumor necrosis factor α; IL-1β: interleukin 1β; IL-6: interleukin 6.

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques: Inhibition, Activity Assay

    The time-dependent impact of LXA4 ( A ), AT-LXA4 ( B ), and MR-39 ( C ) on LPS-induced LDH release in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.01 μM or 0.1 μM), AT-LXA4 (0.01 μM or 0.1 μM), or MR-39 (1 or 5 μM) was added for 1 h, and then the cells were stimulated for 3 or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: The time-dependent impact of LXA4 ( A ), AT-LXA4 ( B ), and MR-39 ( C ) on LPS-induced LDH release in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.01 μM or 0.1 μM), AT-LXA4 (0.01 μM or 0.1 μM), or MR-39 (1 or 5 μM) was added for 1 h, and then the cells were stimulated for 3 or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques:

    The impact of LXA4, AT-LXA4, and MR-39 on the mitochondrial membrane potential ( A ) and caspase-3 activity ( B ) in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: The impact of LXA4, AT-LXA4, and MR-39 on the mitochondrial membrane potential ( A ) and caspase-3 activity ( B ) in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques: Activity Assay

    The impact of LXA4, AT-LXA4, and MR-39 on anti-inflammatory cytokines (IL-10) production in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment-. LXA4: lipoxin A4; AT-LXA4: aspirin-triggered lipoxin A4; LPS: lipopolysaccharide; IL-10: interleukin 10.

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: The impact of LXA4, AT-LXA4, and MR-39 on anti-inflammatory cytokines (IL-10) production in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment-. LXA4: lipoxin A4; AT-LXA4: aspirin-triggered lipoxin A4; LPS: lipopolysaccharide; IL-10: interleukin 10.

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques:

    Representative fluorescence images of microglial cells acquired by confocal microscopy 3 h ( A ) and 24 h ( B ) after FPR2 agonists ((LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM)) and/or lipopolysaccharide (LPS; 0.1 μg/mL) stimulation. Fluorescence intensity of the FPR2 receptor was calculated from images recorded with the use of a fluorescent confocal microscope. Data are derived for control microglia and microglia activated by LPS after 3 h ( C ) and 24 h ( D ) of treatment. Bars present the mean intensity value normalized to the control ± SEM. Nuclei appear in blue, FPR2 in red, and AlexaFluor 488-labeled phalloidin for F-actin in green. Scale bar: 20 μm is located in the bottom right corner of each image. * p

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: Representative fluorescence images of microglial cells acquired by confocal microscopy 3 h ( A ) and 24 h ( B ) after FPR2 agonists ((LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM)) and/or lipopolysaccharide (LPS; 0.1 μg/mL) stimulation. Fluorescence intensity of the FPR2 receptor was calculated from images recorded with the use of a fluorescent confocal microscope. Data are derived for control microglia and microglia activated by LPS after 3 h ( C ) and 24 h ( D ) of treatment. Bars present the mean intensity value normalized to the control ± SEM. Nuclei appear in blue, FPR2 in red, and AlexaFluor 488-labeled phalloidin for F-actin in green. Scale bar: 20 μm is located in the bottom right corner of each image. * p

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques: Fluorescence, Confocal Microscopy, Microscopy, Derivative Assay, Labeling

    The impact of LXA4, AT-LXA4, and MR-39 on pro-inflammatory cytokines: TNF-α ( A ) and IL-1β ( B ) production in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: The impact of LXA4, AT-LXA4, and MR-39 on pro-inflammatory cytokines: TNF-α ( A ) and IL-1β ( B ) production in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques:

    The impact of LXA4 and AT-LXA4 and MR-39 on IL-6 production in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), or AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: The impact of LXA4 and AT-LXA4 and MR-39 on IL-6 production in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), or AT-LXA4 (0.1 μM), or MR-39 (1 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of the control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques:

    The impact of LXA4, AT-LXA4, and MR-39 on reactive oxygen species ( A ) and nitric oxide ( B ) release in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM or 5 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Journal: Cells

    Article Title: Time-Dependent Protective and Pro-Resolving Effects of FPR2 Agonists on Lipopolysaccharide-Exposed Microglia Cells Involve Inhibition of NF-κB and MAPKs Pathways

    doi: 10.3390/cells10092373

    Figure Lengend Snippet: The impact of LXA4, AT-LXA4, and MR-39 on reactive oxygen species ( A ) and nitric oxide ( B ) release in rat microglial cultures. The cells were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). After that, LXA4 (0.1 μM), AT-LXA4 (0.1 μM), or MR-39 (1 μM or 5 μM) was added for 1 h, and then the cells were stimulated for 3 h or 24 h with lipopolysaccharide (LPS; 0.1 μg/mL). Control cultures were treated with the appropriate vehicle. The data are presented as the mean ± SEM percentage of control (vehicle-treated cells) of independent experiments, n = 2–5 in each experiment. * p

    Article Snippet: The FPR2 antagonist WRW4 was purchased from Alomone Labs, Israel.

    Techniques:

    Cell viability and antiviral activity of the anti-FPR2 mAb ( A ) A549 cells were incubated with 10 or 20 µg/mL of the anti-FPR2 mAb for 24 h, and percentage of cell viability was assessed by trypan blue staining; ( B ) A549 cells were preincubated with 20 µg/mL of anti-FPR2 mAb or 5 µM of the FPR2 antagonist WRW4 and then infected with IAV A/PR/8/34 virus (MOI 1). 24 h after infection, infectious virus titers were determined by plaque assay. The Manne Whitney test was used for statistical analysis and results were considered statistically significant at p

    Journal: International Journal of Molecular Sciences

    Article Title: The Annexin A1 Receptor FPR2 Regulates the Endosomal Export of Influenza Virus

    doi: 10.3390/ijms19051400

    Figure Lengend Snippet: Cell viability and antiviral activity of the anti-FPR2 mAb ( A ) A549 cells were incubated with 10 or 20 µg/mL of the anti-FPR2 mAb for 24 h, and percentage of cell viability was assessed by trypan blue staining; ( B ) A549 cells were preincubated with 20 µg/mL of anti-FPR2 mAb or 5 µM of the FPR2 antagonist WRW4 and then infected with IAV A/PR/8/34 virus (MOI 1). 24 h after infection, infectious virus titers were determined by plaque assay. The Manne Whitney test was used for statistical analysis and results were considered statistically significant at p

    Article Snippet: The following reagents were used in this study: antiviral M2 protein (Santa Cruz, Heidelberg, Germany), Alexa Fluor secondary antibodies (Life Technologies, Villebon-sur-Yvette, France), DAPI (4′,6′-diamidino-2-phenylindole, Sigma-Aldrich, Darmstadt, Germany), phalloidin (Invitrogen, Villebon-sur-Yvette, France), purple crystal staining (Sigma, Darmstadt, Germany), FPR2 antagonists WRW4 (Alomone Labs, Jerusalem, Israel), monoclonal anti-FPR2 antibody (clone FN-1D6-AI, Genova, Italy), monoclonal anti-Nucleoprotein (NP, HB-65, invivomab), conjugated Alexa Fluor 488 anti-Rab5 antibody (Santa Cruz, Heidelberg, Germany), IgG control antibody (ThermoFisher, Villebon-sur-Yvette, France), ERK inhibitor pathway U0126 (Sigma-Aldrich, Darmstadt, Germany).

    Techniques: Activity Assay, Incubation, Staining, Infection, Plaque Assay