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mapk signaling pathway inhibitor  (MedChemExpress)


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    MedChemExpress mapk signaling pathway inhibitor
    Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated <t>MAPK</t> to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated <t>using</t> <t>β-actin</t> as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001
    Mapk Signaling Pathway Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 5 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hy-n1966/(E)-Osmundacetone/pm37501100-81-24-31
    Average 94 stars, based on 5 article reviews
    mapk signaling pathway inhibitor - by Bioz Stars, 2026-10
    94/100 stars

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    1) Product Images from "A frog peptide provides new strategies for the intervention against skin wound healing."

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing.

    Journal: Cellular & molecular biology letters

    doi: 10.1186/s11658-023-00468-3

    Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated MAPK to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated using β-actin as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001
    Figure Legend Snippet: Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated MAPK to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated using β-actin as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Techniques Used: Activation Assay, Expressing, Migration, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Western Blot

    Fig. 5 OA-RD17 suppressed inflammatory factor expression and activated the MAPK signaling pathway to promote keratinocyte proliferation and migration. A, B ELISA analysis of effects of OA-RD17 on inflammatory factors (IL-6 and TNF-α) release in keratinocytes after LPS stimulation. C Representative image of MAPK signaling pathway activation in keratinocytes after 24 h of OA-RD17 treatment, determined by western blotting. D Quantification of P38, ERK, and JNK protein phosphorylation. E–G RT-qPCR analysis of Ki67, CDK2, and Cyclin A1 mRNA expression in OA-RD17-treated keratinocytes. H Changes in pro-proliferation activity of OA-RD17 in keratinocytes after application of MAPK signaling pathway inhibitors. I Representative images of effects of OA-RD17 on keratinocyte scratch repair after application of MAPK signaling pathway inhibitors. J Quantification of effects of OA-RD17 on keratinocyte scratch repair rate after application of MAPK signaling pathway inhibitors. All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001
    Figure Legend Snippet: Fig. 5 OA-RD17 suppressed inflammatory factor expression and activated the MAPK signaling pathway to promote keratinocyte proliferation and migration. A, B ELISA analysis of effects of OA-RD17 on inflammatory factors (IL-6 and TNF-α) release in keratinocytes after LPS stimulation. C Representative image of MAPK signaling pathway activation in keratinocytes after 24 h of OA-RD17 treatment, determined by western blotting. D Quantification of P38, ERK, and JNK protein phosphorylation. E–G RT-qPCR analysis of Ki67, CDK2, and Cyclin A1 mRNA expression in OA-RD17-treated keratinocytes. H Changes in pro-proliferation activity of OA-RD17 in keratinocytes after application of MAPK signaling pathway inhibitors. I Representative images of effects of OA-RD17 on keratinocyte scratch repair after application of MAPK signaling pathway inhibitors. J Quantification of effects of OA-RD17 on keratinocyte scratch repair rate after application of MAPK signaling pathway inhibitors. All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Techniques Used: Expressing, Migration, Enzyme-linked Immunosorbent Assay, Activation Assay, Western Blot, Phospho-proteomics, Quantitative RT-PCR, Activity Assay

    Fig. 6 OA-RD17 promoted keratinocyte proliferation and migration via MAPK signaling pathway activation by TLR4. A Representative image of molecular docking of OA-RD17 with TLR4. B Representative images of immunofluorescence for co-localization of TLR4 and OA-RD17 in keratinocytes after treatment with FITC-labeled OA-RD17 for 1 h; green fluorescence for FITC-labeled OA-RD17, red fluorescence for TLR4, and DAPI blue for nuclei; the white arrows indicated the binding of TLR4 and OA-RD17; scale bar 50 µm. C Changes in pro-proliferative activity of OA-RD17 on keratinocytes 24 h after TLR4 inhibition. D Representative images of the effects of OA-RD17 on keratinocyte scratch healing after TLR4 inhibitor treatment. E Quantification of pro-keratinocyte scratch repair by OA-RD17 after TLR4 inhibition. F Western blot analysis of MAPK signaling pathway activation in OA-RD17-treated keratinocytes 24 h after TLR4 inhibition. G–I Quantification of OA-RD17-activated MAPK signaling pathway (P38, ERK, and JNK phosphorylation) in keratinocytes. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001
    Figure Legend Snippet: Fig. 6 OA-RD17 promoted keratinocyte proliferation and migration via MAPK signaling pathway activation by TLR4. A Representative image of molecular docking of OA-RD17 with TLR4. B Representative images of immunofluorescence for co-localization of TLR4 and OA-RD17 in keratinocytes after treatment with FITC-labeled OA-RD17 for 1 h; green fluorescence for FITC-labeled OA-RD17, red fluorescence for TLR4, and DAPI blue for nuclei; the white arrows indicated the binding of TLR4 and OA-RD17; scale bar 50 µm. C Changes in pro-proliferative activity of OA-RD17 on keratinocytes 24 h after TLR4 inhibition. D Representative images of the effects of OA-RD17 on keratinocyte scratch healing after TLR4 inhibitor treatment. E Quantification of pro-keratinocyte scratch repair by OA-RD17 after TLR4 inhibition. F Western blot analysis of MAPK signaling pathway activation in OA-RD17-treated keratinocytes 24 h after TLR4 inhibition. G–I Quantification of OA-RD17-activated MAPK signaling pathway (P38, ERK, and JNK phosphorylation) in keratinocytes. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Techniques Used: Migration, Activation Assay, Immunofluorescence, Labeling, Fluorescence, Binding Assay, Activity Assay, Inhibition, Western Blot, Phospho-proteomics

    Fig. 7 MiR-632 promoted β-catenin expression by targeting GSK3β and activated the Wnt/β-catenin signaling pathway to promote keratinocyte proliferation and migration. A Changes in miR-632 expression in OA-RD17-treated keratinocytes after application of MAPK signaling pathway inhibitors for 24 h, detected by RT-qPCR. B Prediction of binding sites of miR-632 to GSK3β. C Luciferase reporter assay of miR-632 targeting GSK3β. D Effects of miR-632 up-regulation on Wnt/β-catenin signaling pathway, detected by western blotting. E Up-regulation of miR-632 expression significantly inhibited expression of GSK3β protein. F–J Up-regulation of miR-632 expression significantly promoted expression of β-catenin, nuclear accumulation of β-catenin, Vimentin, Cyclin D1, and c-MYC proteins. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, ***P < 0.001, and ****P < 0.0001
    Figure Legend Snippet: Fig. 7 MiR-632 promoted β-catenin expression by targeting GSK3β and activated the Wnt/β-catenin signaling pathway to promote keratinocyte proliferation and migration. A Changes in miR-632 expression in OA-RD17-treated keratinocytes after application of MAPK signaling pathway inhibitors for 24 h, detected by RT-qPCR. B Prediction of binding sites of miR-632 to GSK3β. C Luciferase reporter assay of miR-632 targeting GSK3β. D Effects of miR-632 up-regulation on Wnt/β-catenin signaling pathway, detected by western blotting. E Up-regulation of miR-632 expression significantly inhibited expression of GSK3β protein. F–J Up-regulation of miR-632 expression significantly promoted expression of β-catenin, nuclear accumulation of β-catenin, Vimentin, Cyclin D1, and c-MYC proteins. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, ***P < 0.001, and ****P < 0.0001

    Techniques Used: Expressing, Migration, Quantitative RT-PCR, Binding Assay, Luciferase, Reporter Assay, Western Blot

    Related Articles

    Migration:

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing.
    Article Snippet: The effects of miR632 mimic (50 nM), miR-632 inhibitor (100 nM) (riboFECTTM CP Transfection Kit, RiboBio, China), and OA-RD17 (1 nM) on keratinocyte migration were determined following the manufacturer’s instructions. .. Additionally, the mechanism of OA-RD17induced macrophage migration was investigated using a specific MAPK signaling pathway inhibitor (10 μM, HY-N1966, MedChemExpress, USA). ..

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing
    Article Snippet: The effects of miR-632 mimic (50 nM), miR-632 inhibitor (100 nM) (riboFECTTM CP Transfection Kit, RiboBio, China), and OA-RD17 (1 nM) on keratinocyte migration were determined following the manufacturer’s instructions. .. Additionally, the mechanism of OA-RD17-induced macrophage migration was investigated using a specific MAPK signaling pathway inhibitor (10 μM, HY-N1966, MedChemExpress, USA). ..



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    Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated <t>MAPK</t> to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated <t>using</t> <t>β-actin</t> as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001
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    Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated <t>MAPK</t> to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated <t>using</t> <t>β-actin</t> as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001
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    Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated MAPK to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated using β-actin as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Journal: Cellular & molecular biology letters

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing.

    doi: 10.1186/s11658-023-00468-3

    Figure Lengend Snippet: Fig. 4 OA-RD17 inhibited NF-κB activation to suppress inflammatory factors expression and activated MAPK to promote macrophage proliferation and migration. A-C RT-qPCR was performed to detect changes in mRNA expression levels of IL-6, IL-1β, and TNF-α in macrophages treated with PBS, LPS, or LPS + OA-RD17. Relative expression was calculated using β-actin as an internal reference. D-F ELISA was conducted to determine IL-6, IL-1β, and TNF-α expression in macrophages treated with PBS, LPS, or LPS + OA-RD17. G OA-RD17 inhibited activation of NF-κB signaling pathway induced by LPS in macrophages. H Quantification of phosphorylation of P65 and IκB. I Western blotting was performed to detect effects of OA-RD17 treatment for 24 h on MAPK signaling pathway in macrophages. J Quantification of key proteins of macrophage MAPK signaling pathway (phosphorylated proteins of P38, ERK, and JNK). All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Article Snippet: In addition, the underlying mechanisms of OA-RD17- and miR-632-induced keratinocyte scratch healing were determined using a specific TLR4 inhibitor (1 μM, HY-11109, MedChemExpress, USA), MAPK signaling pathway inhibitor (1 μM, HY-N1966, MedChemExpress, USA), or β-catenin inhibitor (10 μM, HY-120697, MedChemExpress, USA).

    Techniques: Activation Assay, Expressing, Migration, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Western Blot

    Fig. 5 OA-RD17 suppressed inflammatory factor expression and activated the MAPK signaling pathway to promote keratinocyte proliferation and migration. A, B ELISA analysis of effects of OA-RD17 on inflammatory factors (IL-6 and TNF-α) release in keratinocytes after LPS stimulation. C Representative image of MAPK signaling pathway activation in keratinocytes after 24 h of OA-RD17 treatment, determined by western blotting. D Quantification of P38, ERK, and JNK protein phosphorylation. E–G RT-qPCR analysis of Ki67, CDK2, and Cyclin A1 mRNA expression in OA-RD17-treated keratinocytes. H Changes in pro-proliferation activity of OA-RD17 in keratinocytes after application of MAPK signaling pathway inhibitors. I Representative images of effects of OA-RD17 on keratinocyte scratch repair after application of MAPK signaling pathway inhibitors. J Quantification of effects of OA-RD17 on keratinocyte scratch repair rate after application of MAPK signaling pathway inhibitors. All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Journal: Cellular & molecular biology letters

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing.

    doi: 10.1186/s11658-023-00468-3

    Figure Lengend Snippet: Fig. 5 OA-RD17 suppressed inflammatory factor expression and activated the MAPK signaling pathway to promote keratinocyte proliferation and migration. A, B ELISA analysis of effects of OA-RD17 on inflammatory factors (IL-6 and TNF-α) release in keratinocytes after LPS stimulation. C Representative image of MAPK signaling pathway activation in keratinocytes after 24 h of OA-RD17 treatment, determined by western blotting. D Quantification of P38, ERK, and JNK protein phosphorylation. E–G RT-qPCR analysis of Ki67, CDK2, and Cyclin A1 mRNA expression in OA-RD17-treated keratinocytes. H Changes in pro-proliferation activity of OA-RD17 in keratinocytes after application of MAPK signaling pathway inhibitors. I Representative images of effects of OA-RD17 on keratinocyte scratch repair after application of MAPK signaling pathway inhibitors. J Quantification of effects of OA-RD17 on keratinocyte scratch repair rate after application of MAPK signaling pathway inhibitors. All data are expressed as mean ± SEM from three independent experiments, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Article Snippet: In addition, the underlying mechanisms of OA-RD17- and miR-632-induced keratinocyte scratch healing were determined using a specific TLR4 inhibitor (1 μM, HY-11109, MedChemExpress, USA), MAPK signaling pathway inhibitor (1 μM, HY-N1966, MedChemExpress, USA), or β-catenin inhibitor (10 μM, HY-120697, MedChemExpress, USA).

    Techniques: Expressing, Migration, Enzyme-linked Immunosorbent Assay, Activation Assay, Western Blot, Phospho-proteomics, Quantitative RT-PCR, Activity Assay

    Fig. 6 OA-RD17 promoted keratinocyte proliferation and migration via MAPK signaling pathway activation by TLR4. A Representative image of molecular docking of OA-RD17 with TLR4. B Representative images of immunofluorescence for co-localization of TLR4 and OA-RD17 in keratinocytes after treatment with FITC-labeled OA-RD17 for 1 h; green fluorescence for FITC-labeled OA-RD17, red fluorescence for TLR4, and DAPI blue for nuclei; the white arrows indicated the binding of TLR4 and OA-RD17; scale bar 50 µm. C Changes in pro-proliferative activity of OA-RD17 on keratinocytes 24 h after TLR4 inhibition. D Representative images of the effects of OA-RD17 on keratinocyte scratch healing after TLR4 inhibitor treatment. E Quantification of pro-keratinocyte scratch repair by OA-RD17 after TLR4 inhibition. F Western blot analysis of MAPK signaling pathway activation in OA-RD17-treated keratinocytes 24 h after TLR4 inhibition. G–I Quantification of OA-RD17-activated MAPK signaling pathway (P38, ERK, and JNK phosphorylation) in keratinocytes. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Journal: Cellular & molecular biology letters

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing.

    doi: 10.1186/s11658-023-00468-3

    Figure Lengend Snippet: Fig. 6 OA-RD17 promoted keratinocyte proliferation and migration via MAPK signaling pathway activation by TLR4. A Representative image of molecular docking of OA-RD17 with TLR4. B Representative images of immunofluorescence for co-localization of TLR4 and OA-RD17 in keratinocytes after treatment with FITC-labeled OA-RD17 for 1 h; green fluorescence for FITC-labeled OA-RD17, red fluorescence for TLR4, and DAPI blue for nuclei; the white arrows indicated the binding of TLR4 and OA-RD17; scale bar 50 µm. C Changes in pro-proliferative activity of OA-RD17 on keratinocytes 24 h after TLR4 inhibition. D Representative images of the effects of OA-RD17 on keratinocyte scratch healing after TLR4 inhibitor treatment. E Quantification of pro-keratinocyte scratch repair by OA-RD17 after TLR4 inhibition. F Western blot analysis of MAPK signaling pathway activation in OA-RD17-treated keratinocytes 24 h after TLR4 inhibition. G–I Quantification of OA-RD17-activated MAPK signaling pathway (P38, ERK, and JNK phosphorylation) in keratinocytes. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, *P < 0.05, **P < 0.01, ***P < 0.001, and ****P < 0.0001

    Article Snippet: In addition, the underlying mechanisms of OA-RD17- and miR-632-induced keratinocyte scratch healing were determined using a specific TLR4 inhibitor (1 μM, HY-11109, MedChemExpress, USA), MAPK signaling pathway inhibitor (1 μM, HY-N1966, MedChemExpress, USA), or β-catenin inhibitor (10 μM, HY-120697, MedChemExpress, USA).

    Techniques: Migration, Activation Assay, Immunofluorescence, Labeling, Fluorescence, Binding Assay, Activity Assay, Inhibition, Western Blot, Phospho-proteomics

    Fig. 7 MiR-632 promoted β-catenin expression by targeting GSK3β and activated the Wnt/β-catenin signaling pathway to promote keratinocyte proliferation and migration. A Changes in miR-632 expression in OA-RD17-treated keratinocytes after application of MAPK signaling pathway inhibitors for 24 h, detected by RT-qPCR. B Prediction of binding sites of miR-632 to GSK3β. C Luciferase reporter assay of miR-632 targeting GSK3β. D Effects of miR-632 up-regulation on Wnt/β-catenin signaling pathway, detected by western blotting. E Up-regulation of miR-632 expression significantly inhibited expression of GSK3β protein. F–J Up-regulation of miR-632 expression significantly promoted expression of β-catenin, nuclear accumulation of β-catenin, Vimentin, Cyclin D1, and c-MYC proteins. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, ***P < 0.001, and ****P < 0.0001

    Journal: Cellular & molecular biology letters

    Article Title: A frog peptide provides new strategies for the intervention against skin wound healing.

    doi: 10.1186/s11658-023-00468-3

    Figure Lengend Snippet: Fig. 7 MiR-632 promoted β-catenin expression by targeting GSK3β and activated the Wnt/β-catenin signaling pathway to promote keratinocyte proliferation and migration. A Changes in miR-632 expression in OA-RD17-treated keratinocytes after application of MAPK signaling pathway inhibitors for 24 h, detected by RT-qPCR. B Prediction of binding sites of miR-632 to GSK3β. C Luciferase reporter assay of miR-632 targeting GSK3β. D Effects of miR-632 up-regulation on Wnt/β-catenin signaling pathway, detected by western blotting. E Up-regulation of miR-632 expression significantly inhibited expression of GSK3β protein. F–J Up-regulation of miR-632 expression significantly promoted expression of β-catenin, nuclear accumulation of β-catenin, Vimentin, Cyclin D1, and c-MYC proteins. All data are expressed as mean ± SEM from three independent experiments, ns, no significance, ***P < 0.001, and ****P < 0.0001

    Article Snippet: In addition, the underlying mechanisms of OA-RD17- and miR-632-induced keratinocyte scratch healing were determined using a specific TLR4 inhibitor (1 μM, HY-11109, MedChemExpress, USA), MAPK signaling pathway inhibitor (1 μM, HY-N1966, MedChemExpress, USA), or β-catenin inhibitor (10 μM, HY-120697, MedChemExpress, USA).

    Techniques: Expressing, Migration, Quantitative RT-PCR, Binding Assay, Luciferase, Reporter Assay, Western Blot