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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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    wrw4 - by Bioz Stars, 2022-12
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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

    MR-39 treatment decreases the synthesis of MyD88 and NF-kB induced by Aβ 1-42 administration in OHCs obtained from the offspring of WT but not KO FPR2 mice. OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

    Journal: Molecular Neurobiology

    Article Title: The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

    doi: 10.1007/s12035-021-02543-2

    Figure Lengend Snippet: MR-39 treatment decreases the synthesis of MyD88 and NF-kB induced by Aβ 1-42 administration in OHCs obtained from the offspring of WT but not KO FPR2 mice. OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

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

    Techniques: Mouse Assay

    MR-39 treatment diminishes the synthesis of NLRP3, caspase-1 and ASC evoked by Aβ 1-42 administration in OHCs obtained from the offspring of WT but not KO FPR2 mice. OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

    Journal: Molecular Neurobiology

    Article Title: The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

    doi: 10.1007/s12035-021-02543-2

    Figure Lengend Snippet: MR-39 treatment diminishes the synthesis of NLRP3, caspase-1 and ASC evoked by Aβ 1-42 administration in OHCs obtained from the offspring of WT but not KO FPR2 mice. OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

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

    Techniques: Mouse Assay

    The influence of oligomeric and fibrillar types of β-amyloid on cell death in OHCs obtained from the offspring of WT and KO FPR2 mice. OHCs were stimulated for 24 h with fibrillar or oligomeric amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The effect of β-amyloid (oligomeric Aβ 1-42 and fibrillar Aβ 1-42 ) on cell death (LDH) was measured. The data are presented as the mean ± SD, percentage of the control values (vehicle-treated WT OHCs) obtained in independent experiments. The results were statistically evaluated using a two-way analysis of variance (ANOVA) with the Duncan post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

    Journal: Molecular Neurobiology

    Article Title: The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

    doi: 10.1007/s12035-021-02543-2

    Figure Lengend Snippet: The influence of oligomeric and fibrillar types of β-amyloid on cell death in OHCs obtained from the offspring of WT and KO FPR2 mice. OHCs were stimulated for 24 h with fibrillar or oligomeric amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The effect of β-amyloid (oligomeric Aβ 1-42 and fibrillar Aβ 1-42 ) on cell death (LDH) was measured. The data are presented as the mean ± SD, percentage of the control values (vehicle-treated WT OHCs) obtained in independent experiments. The results were statistically evaluated using a two-way analysis of variance (ANOVA) with the Duncan post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

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

    Techniques: Mouse Assay

    MR-39 treatment diminishes Aβ 1-42 -induced LDH release in OHCs from the offspring of WT but not KO FPR2 mice. OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. NO release was measured by the Griess reaction. The data are presented as the mean ± SD, percentage of the control values (vehicle-treated WT OHCs) obtained in independent experiments. The results were statistically evaluated using a two-way analysis of variance (ANOVA) with the Duncan post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

    Journal: Molecular Neurobiology

    Article Title: The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

    doi: 10.1007/s12035-021-02543-2

    Figure Lengend Snippet: MR-39 treatment diminishes Aβ 1-42 -induced LDH release in OHCs from the offspring of WT but not KO FPR2 mice. OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. NO release was measured by the Griess reaction. The data are presented as the mean ± SD, percentage of the control values (vehicle-treated WT OHCs) obtained in independent experiments. The results were statistically evaluated using a two-way analysis of variance (ANOVA) with the Duncan post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

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

    Techniques: Mouse Assay

    MR-39 treatment increases the release of anti-inflammatory cytokines in OHCs obtained from the offspring of WT but not KO FPR2 mice. OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

    Journal: Molecular Neurobiology

    Article Title: The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

    doi: 10.1007/s12035-021-02543-2

    Figure Lengend Snippet: MR-39 treatment increases the release of anti-inflammatory cytokines in OHCs obtained from the offspring of WT but not KO FPR2 mice. OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

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

    Techniques: Mouse Assay

    MR-39 treatment diminishes proinflammatory cytokine release evoked by Aβ 1-42 treatment in OHCs from the offspring of WT but not KO FPR2 mice . OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

    Journal: Molecular Neurobiology

    Article Title: The N-Formyl Peptide Receptor 2 (FPR2) Agonist MR-39 Improves Ex Vivo and In Vivo Amyloid Beta (1–42)-Induced Neuroinflammation in Mouse Models of Alzheimer’s Disease

    doi: 10.1007/s12035-021-02543-2

    Figure Lengend Snippet: MR-39 treatment diminishes proinflammatory cytokine release evoked by Aβ 1-42 treatment in OHCs from the offspring of WT but not KO FPR2 mice . OHCs were pretreated for 30 min with the FPR2 antagonist WRW4 (10 µM). Then, MR-39 (1 µM) was added for 1 h, and OHCs were stimulated for 24 h with fibrillar amyloid β (Aβ 1-42 ; 10 μM). Control cultures were treated with the appropriate vehicle. The results are expressed as the mean ± SD. The data are from independent experiments. The results were statistically evaluated using factorial analysis of variance (ANOVA) with Duncan’s post hoc test to assess the differences between the treatment groups. Significant differences are indicated by ∗ p

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

    Techniques: Mouse 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