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osm  (Bioss)


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    Bioss osm
    Osm, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/osm/product/Bioss
    Average 94 stars, based on 1 article reviews
    osm - by Bioz Stars, 2026-02
    94/100 stars

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    Representative microscopic images of cells cultured <t>with</t> <t>OSM</t> stimulation in Control, Mock, and OSMRβ-overexpressing cell lines. (A) Control/OSM-, (B) Control/OSM+, (C) Mock/OSM-, (D) Mock/OSM+, (E) OSMRβ overexpressing/OSM-, (F) OSMRβ overexpressing/OSM+. Results of neurite length measurements and statistical evaluation after OSM stimulation of Control, Mock, and OSMRβ-overexpressing cell lines (G) . Data are presented as the mean ± standard error (SE), * p <0.05, **** p <0.0001. For each condition, 9–11 random fields were imaged, and the five longest neurites per field were measured. The experiment was repeated in triplicate, and the data were combined for analysis. OSM, oncostatin M; <t>OSMR,</t> oncostatin M receptor.
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    Image Search Results


    OSM promotes IL-4 production in airway fibroblasts. ( A-B ) IL-4 expression profiles in fibroblast lines following 48 hr OSM exposure. ( C ) OSMR knockdown efficiency in WI-38 cells. ( D-E ) IL-4 mRNA ( D ) and protein ( E ) levels after OSMR RNAi. ( F-G ) In vivo OSM administration (7 days): IL-4 mRNA in lung fibroblasts ( F ) and protein in lung homogenates (G). Data shown as mean ± SD with individual points. Statistical analysis: ANOVA with Tukey’s test; * p <0.05; ** p <0.01; *** p <0.001; **** p <0.0001. RE: Relative expression.

    Journal: International Journal of Nanomedicine

    Article Title: Oncostatin M Drives Th2 Polarized Allergic Airway Inflammation Through Fibroblast Reprogramming and Endoplasmic Reticulum Stress

    doi: 10.2147/IJN.S535265

    Figure Lengend Snippet: OSM promotes IL-4 production in airway fibroblasts. ( A-B ) IL-4 expression profiles in fibroblast lines following 48 hr OSM exposure. ( C ) OSMR knockdown efficiency in WI-38 cells. ( D-E ) IL-4 mRNA ( D ) and protein ( E ) levels after OSMR RNAi. ( F-G ) In vivo OSM administration (7 days): IL-4 mRNA in lung fibroblasts ( F ) and protein in lung homogenates (G). Data shown as mean ± SD with individual points. Statistical analysis: ANOVA with Tukey’s test; * p <0.05; ** p <0.01; *** p <0.001; **** p <0.0001. RE: Relative expression.

    Article Snippet: Fibroblast treatment: WI-38 and MRC-5 cells (ATCC) were stimulated with OSM (10–100 nM) for 48 hours or transfected with OSMR siRNA (Santa Cruz, sc-137176) using Lipofectamine 3000 (Invitrogen).

    Techniques: Expressing, Knockdown, In Vivo

    Transcriptomic profiling of OSM-activated airway fibroblasts. Lung fibroblasts from OSM- or PBS-treated mice (n=6/group) underwent RNA sequencing. ( A ) Volcano plot of differentially expressed genes (DEGs). ( B-C ) Th2-associated biological processes ( B ) and enriched pathways (C, red boxes). ( D ) Violin plot of Il4 expression. ( E-H ) Protein levels of endoplasmic reticulum stress (ERS) markers and IL-4. ( I ) Correlation heatmap between fibroblast parameters and BALF components. Data presented as mean ± SD ( D and E ) with individual points. Statistics: Student’s t -test ( D and E ) and Pearson’s correlation (F). * p <0.05. ** p <0.01; *** p<0.001 . Raw data (A-D): BioProject PRJNA11112352; SRA SRP508146. Abbreviations: IL-4/IL-5/IL-13 (samples from OSM-treated mice); p-PERK/p-eIF2α (phosphorylated forms); n-ATF4 (nuclear translocated); GSK (PERK inhibitor GSK2606414, 0.4 nM).

    Journal: International Journal of Nanomedicine

    Article Title: Oncostatin M Drives Th2 Polarized Allergic Airway Inflammation Through Fibroblast Reprogramming and Endoplasmic Reticulum Stress

    doi: 10.2147/IJN.S535265

    Figure Lengend Snippet: Transcriptomic profiling of OSM-activated airway fibroblasts. Lung fibroblasts from OSM- or PBS-treated mice (n=6/group) underwent RNA sequencing. ( A ) Volcano plot of differentially expressed genes (DEGs). ( B-C ) Th2-associated biological processes ( B ) and enriched pathways (C, red boxes). ( D ) Violin plot of Il4 expression. ( E-H ) Protein levels of endoplasmic reticulum stress (ERS) markers and IL-4. ( I ) Correlation heatmap between fibroblast parameters and BALF components. Data presented as mean ± SD ( D and E ) with individual points. Statistics: Student’s t -test ( D and E ) and Pearson’s correlation (F). * p <0.05. ** p <0.01; *** p<0.001 . Raw data (A-D): BioProject PRJNA11112352; SRA SRP508146. Abbreviations: IL-4/IL-5/IL-13 (samples from OSM-treated mice); p-PERK/p-eIF2α (phosphorylated forms); n-ATF4 (nuclear translocated); GSK (PERK inhibitor GSK2606414, 0.4 nM).

    Article Snippet: Fibroblast treatment: WI-38 and MRC-5 cells (ATCC) were stimulated with OSM (10–100 nM) for 48 hours or transfected with OSMR siRNA (Santa Cruz, sc-137176) using Lipofectamine 3000 (Invitrogen).

    Techniques: RNA Sequencing, Expressing

    Synergistic activation of IL-4 promoter by ATF4-Mef2d-GATA3 axis.A, the amount of phosphorylated PERK (pPERK) in lung fibroblasts. ( B and C ) Immunoprecipitation showing ATF4-Mef2d interaction in lung fibroblasts from OSM-treated mice. ( D ) Predicted ATF4-Mef2d complex structure. ( E ) Confocal microscopy (630×) of subcellular His-Mef2d localization (in green) in ATF4-transfected HEK293 cells (the nuclei were stained with propidium iodide in red). ( F–H ) Cytoplasm Mef2d (F), nuclear Mef2d ( G ) and GATA3 ( H ) levels. E235 (5 µM; MCE): An inhibitor of ATF4. ( I ) Luciferase reporter assay of IL-4 promoter activation (A: ATF4; ( M ) Mef2d; ( G ) GATA3; muA: ATF4 mutant). ( J–K ) IL-4 mRNA ( I ) and protein ( J ) levels. GSK: (GSK2606414; 0.4 nM; MCE): An inhibitor of PERK. Data shown as mean ± SD with individual points. Statistical analysis: ANOVA with Tukey’s test; * p <0.05; ** p <0.01; *** p <0.001; **** p <0.0001. OD: Optical density.

    Journal: International Journal of Nanomedicine

    Article Title: Oncostatin M Drives Th2 Polarized Allergic Airway Inflammation Through Fibroblast Reprogramming and Endoplasmic Reticulum Stress

    doi: 10.2147/IJN.S535265

    Figure Lengend Snippet: Synergistic activation of IL-4 promoter by ATF4-Mef2d-GATA3 axis.A, the amount of phosphorylated PERK (pPERK) in lung fibroblasts. ( B and C ) Immunoprecipitation showing ATF4-Mef2d interaction in lung fibroblasts from OSM-treated mice. ( D ) Predicted ATF4-Mef2d complex structure. ( E ) Confocal microscopy (630×) of subcellular His-Mef2d localization (in green) in ATF4-transfected HEK293 cells (the nuclei were stained with propidium iodide in red). ( F–H ) Cytoplasm Mef2d (F), nuclear Mef2d ( G ) and GATA3 ( H ) levels. E235 (5 µM; MCE): An inhibitor of ATF4. ( I ) Luciferase reporter assay of IL-4 promoter activation (A: ATF4; ( M ) Mef2d; ( G ) GATA3; muA: ATF4 mutant). ( J–K ) IL-4 mRNA ( I ) and protein ( J ) levels. GSK: (GSK2606414; 0.4 nM; MCE): An inhibitor of PERK. Data shown as mean ± SD with individual points. Statistical analysis: ANOVA with Tukey’s test; * p <0.05; ** p <0.01; *** p <0.001; **** p <0.0001. OD: Optical density.

    Article Snippet: Fibroblast treatment: WI-38 and MRC-5 cells (ATCC) were stimulated with OSM (10–100 nM) for 48 hours or transfected with OSMR siRNA (Santa Cruz, sc-137176) using Lipofectamine 3000 (Invitrogen).

    Techniques: Activation Assay, Immunoprecipitation, Confocal Microscopy, Transfection, Staining, Luciferase, Reporter Assay, Mutagenesis

    Representative microscopic images of cells cultured with OSM stimulation in Control, Mock, and OSMRβ-overexpressing cell lines. (A) Control/OSM-, (B) Control/OSM+, (C) Mock/OSM-, (D) Mock/OSM+, (E) OSMRβ overexpressing/OSM-, (F) OSMRβ overexpressing/OSM+. Results of neurite length measurements and statistical evaluation after OSM stimulation of Control, Mock, and OSMRβ-overexpressing cell lines (G) . Data are presented as the mean ± standard error (SE), * p <0.05, **** p <0.0001. For each condition, 9–11 random fields were imaged, and the five longest neurites per field were measured. The experiment was repeated in triplicate, and the data were combined for analysis. OSM, oncostatin M; OSMR, oncostatin M receptor.

    Journal: Frontiers in Immunology

    Article Title: Oncostatin M enhances the lengthening of sensory nerves and skin hypersensitivity

    doi: 10.3389/fimmu.2025.1571120

    Figure Lengend Snippet: Representative microscopic images of cells cultured with OSM stimulation in Control, Mock, and OSMRβ-overexpressing cell lines. (A) Control/OSM-, (B) Control/OSM+, (C) Mock/OSM-, (D) Mock/OSM+, (E) OSMRβ overexpressing/OSM-, (F) OSMRβ overexpressing/OSM+. Results of neurite length measurements and statistical evaluation after OSM stimulation of Control, Mock, and OSMRβ-overexpressing cell lines (G) . Data are presented as the mean ± standard error (SE), * p <0.05, **** p <0.0001. For each condition, 9–11 random fields were imaged, and the five longest neurites per field were measured. The experiment was repeated in triplicate, and the data were combined for analysis. OSM, oncostatin M; OSMR, oncostatin M receptor.

    Article Snippet: Primer pairs for detecting OSM, the OSMR, were obtained from ThermoFisher Scientific.

    Techniques: Cell Culture, Control