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wnt2b  (Cusabio)


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    Cusabio wnt2b
    MSC(SG), particularly after cytokine pre-licensing with IFNγ and TNFα, are a feasible and enhanced MSC source for treatment of radiation-induced xerostomia. Bulk RNA sequencing of MSC(BM), MSC(AD), and MSC(SG) revealed that they shared 85 % of transcripts. Key differences included extracellular matrix production and response to cytokines in MSC(SG). Regardless of MSC source, dual stimulation of MSCs with IFNγ and TNFα produced an average of more than a 20-fold increase in R-Spondin 3 compared to vehicle conditions. Additionally, IFNγ and TNFα pre-licensing optimized immunomodulatory marker expression more than IFNγ alone. Intercellular adhesion molecule 1 (ICAM-1) increased 12-fold more, programmed death ligand 1 (PD-L1) increased 1.4-fold more, and indoleamine 2,3 dioxygenase (IDO) increased 2-fold more with IFNγ/TNFα pre-licensing than IFNγ alone. Both cytokine stimulation conditions resulted in a 1.2-fold decrease in T-cell proliferation. Gland structure and salivary flow are preserved in irradiated mice treated with MSC(SG) pre-licensed with IFNγ/TNFα. B) proposed mechanism of MSC action. R-Spondin 3 and <t>Wnt2b</t> generated by MSC(SG) promote epithelial regeneration after damage from radiation. Radiation also creates a pro-inflammatory local environment with increased dual positive T cells. MSC(SG) might protect local epithelial through optimizing the local inflammatory milieu like protecting macrophages that are important for tissue repair. McCoy, S. (2025) https://BioRender.com/o01d792 . Created in https://BioRender.com .
    Wnt2b, supplied by Cusabio, used in various techniques. Bioz Stars score: 93/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/wnt2b/WNT2B/pmc12663032-95-30-31
    Average 93 stars, based on 4 article reviews
    wnt2b - by Bioz Stars, 2026-11
    93/100 stars

    Images

    1) Product Images from "IFNγ and TNFα optimize salivary gland mesenchymal stromal cells: an alternative to marrow- and adipose-MSCs for radiation xerostomia"

    Article Title: IFNγ and TNFα optimize salivary gland mesenchymal stromal cells: an alternative to marrow- and adipose-MSCs for radiation xerostomia

    Journal: Regenerative Therapy

    doi: 10.1016/j.reth.2025.11.004

    MSC(SG), particularly after cytokine pre-licensing with IFNγ and TNFα, are a feasible and enhanced MSC source for treatment of radiation-induced xerostomia. Bulk RNA sequencing of MSC(BM), MSC(AD), and MSC(SG) revealed that they shared 85 % of transcripts. Key differences included extracellular matrix production and response to cytokines in MSC(SG). Regardless of MSC source, dual stimulation of MSCs with IFNγ and TNFα produced an average of more than a 20-fold increase in R-Spondin 3 compared to vehicle conditions. Additionally, IFNγ and TNFα pre-licensing optimized immunomodulatory marker expression more than IFNγ alone. Intercellular adhesion molecule 1 (ICAM-1) increased 12-fold more, programmed death ligand 1 (PD-L1) increased 1.4-fold more, and indoleamine 2,3 dioxygenase (IDO) increased 2-fold more with IFNγ/TNFα pre-licensing than IFNγ alone. Both cytokine stimulation conditions resulted in a 1.2-fold decrease in T-cell proliferation. Gland structure and salivary flow are preserved in irradiated mice treated with MSC(SG) pre-licensed with IFNγ/TNFα. B) proposed mechanism of MSC action. R-Spondin 3 and Wnt2b generated by MSC(SG) promote epithelial regeneration after damage from radiation. Radiation also creates a pro-inflammatory local environment with increased dual positive T cells. MSC(SG) might protect local epithelial through optimizing the local inflammatory milieu like protecting macrophages that are important for tissue repair. McCoy, S. (2025) https://BioRender.com/o01d792 . Created in https://BioRender.com .
    Figure Legend Snippet: MSC(SG), particularly after cytokine pre-licensing with IFNγ and TNFα, are a feasible and enhanced MSC source for treatment of radiation-induced xerostomia. Bulk RNA sequencing of MSC(BM), MSC(AD), and MSC(SG) revealed that they shared 85 % of transcripts. Key differences included extracellular matrix production and response to cytokines in MSC(SG). Regardless of MSC source, dual stimulation of MSCs with IFNγ and TNFα produced an average of more than a 20-fold increase in R-Spondin 3 compared to vehicle conditions. Additionally, IFNγ and TNFα pre-licensing optimized immunomodulatory marker expression more than IFNγ alone. Intercellular adhesion molecule 1 (ICAM-1) increased 12-fold more, programmed death ligand 1 (PD-L1) increased 1.4-fold more, and indoleamine 2,3 dioxygenase (IDO) increased 2-fold more with IFNγ/TNFα pre-licensing than IFNγ alone. Both cytokine stimulation conditions resulted in a 1.2-fold decrease in T-cell proliferation. Gland structure and salivary flow are preserved in irradiated mice treated with MSC(SG) pre-licensed with IFNγ/TNFα. B) proposed mechanism of MSC action. R-Spondin 3 and Wnt2b generated by MSC(SG) promote epithelial regeneration after damage from radiation. Radiation also creates a pro-inflammatory local environment with increased dual positive T cells. MSC(SG) might protect local epithelial through optimizing the local inflammatory milieu like protecting macrophages that are important for tissue repair. McCoy, S. (2025) https://BioRender.com/o01d792 . Created in https://BioRender.com .

    Techniques Used: RNA Sequencing, Produced, Marker, Expressing, Irradiation, Generated

    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: IFNγ and TNFα optimize salivary gland mesenchymal stromal cells: an alternative to marrow- and adipose-MSCs for radiation xerostomia
    Article Snippet: To establish the trophic secretome, MSC(BM) (n = 3), MSC(AD) (n = 3), and MSC(SG) (n = 9) were treated with IFNγ (10 ng/mL)); PeproTech, Cranbury, NJ), TNFα (10 ng/mL; BioLegend, San Diego, CA), or TGFβ (2.5 ng/mL; PeproTech, Cranbury, NJ). .. After 48 h of culture, the conditioned media was used for ELISA per the manufacturer's recommendations (GDNF [Innovative Research Novi MI], RSPO1 [CUSABIO, Houston, TX], RSPO3 [Innovative Research], Wnt1 [CUSABIO], Wnt2b [CUSABIO], Wnt3a [CUSABIO], Wnt4 [Raybiotech, Norcross, GA], Wnt5a [CUSABIO]) with dilutions described in the Supplemental Methods. .. To establish the trophic secretome, MSC(BM) (n = 3), MSC(AD) (n = 3), and MSC(SG) (n = 9) were treated with IFNγ (10 ng/mL)); PeproTech, Cranbury, NJ), TNFα (10 ng/mL; BioLegend, San Diego, CA), or TGFβ (2.5 ng/mL; PeproTech, Cranbury, NJ).

    Article Title: Downregulation of the Canonical WNT Signaling Pathway by TGFβ1 Inhibits Photoreceptor Differentiation of Adult Human Müller Glia with Stem Cell Characteristics
    Article Snippet: .. Supernatants were collected and used for Enzyme-Linked Immunosorbent Assay (ELISA) analysis for quantification of secreted DKK1 (R&D Systems), WNT2B, and WNT5B (CUSABIO) using the manufacturer's instructions. ..

    Article Title: Downregulation of the Canonical WNT Signaling Pathway by TGFβ1 Inhibits Photoreceptor Differentiation of Adult Human Müller Glia with Stem Cell Characteristics.
    Article Snippet: Enzyme-Linked Immunosorbent Assay The hMSC were grown for 5–6 days in DMEM with 2% FCS on bMP-coated flasks in the presence or absence of either human recombinant TGFb1 (50 ng/mL) or FTRI to induce photoreceptor differentiation as indicated above [3]. .. Supernatants were collected and used for Enzyme-Linked Immunosorbent Assay (ELISA) analysis for quantification of secreted DKK1 (R&D Systems), WNT2B, and WNT5B (CUSABIO) using the manufacturer’s instructions. ..

    Analysis:

    Article Title: Downregulation of the Canonical WNT Signaling Pathway by TGFβ1 Inhibits Photoreceptor Differentiation of Adult Human Müller Glia with Stem Cell Characteristics
    Article Snippet: .. Supernatants were collected and used for Enzyme-Linked Immunosorbent Assay (ELISA) analysis for quantification of secreted DKK1 (R&D Systems), WNT2B, and WNT5B (CUSABIO) using the manufacturer's instructions. ..



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    MSC(SG), particularly after cytokine pre-licensing with IFNγ and TNFα, are a feasible and enhanced MSC source for treatment of radiation-induced xerostomia. Bulk RNA sequencing of MSC(BM), MSC(AD), and MSC(SG) revealed that they shared 85 % of transcripts. Key differences included extracellular matrix production and response to cytokines in MSC(SG). Regardless of MSC source, dual stimulation of MSCs with IFNγ and TNFα produced an average of more than a 20-fold increase in R-Spondin 3 compared to vehicle conditions. Additionally, IFNγ and TNFα pre-licensing optimized immunomodulatory marker expression more than IFNγ alone. Intercellular adhesion molecule 1 (ICAM-1) increased 12-fold more, programmed death ligand 1 (PD-L1) increased 1.4-fold more, and indoleamine 2,3 dioxygenase (IDO) increased 2-fold more with IFNγ/TNFα pre-licensing than IFNγ alone. Both cytokine stimulation conditions resulted in a 1.2-fold decrease in T-cell proliferation. Gland structure and salivary flow are preserved in irradiated mice treated with MSC(SG) pre-licensed with IFNγ/TNFα. B) proposed mechanism of MSC action. R-Spondin 3 and <t>Wnt2b</t> generated by MSC(SG) promote epithelial regeneration after damage from radiation. Radiation also creates a pro-inflammatory local environment with increased dual positive T cells. MSC(SG) might protect local epithelial through optimizing the local inflammatory milieu like protecting macrophages that are important for tissue repair. McCoy, S. (2025) https://BioRender.com/o01d792 . Created in https://BioRender.com .
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    Image Search Results


    MSC(SG), particularly after cytokine pre-licensing with IFNγ and TNFα, are a feasible and enhanced MSC source for treatment of radiation-induced xerostomia. Bulk RNA sequencing of MSC(BM), MSC(AD), and MSC(SG) revealed that they shared 85 % of transcripts. Key differences included extracellular matrix production and response to cytokines in MSC(SG). Regardless of MSC source, dual stimulation of MSCs with IFNγ and TNFα produced an average of more than a 20-fold increase in R-Spondin 3 compared to vehicle conditions. Additionally, IFNγ and TNFα pre-licensing optimized immunomodulatory marker expression more than IFNγ alone. Intercellular adhesion molecule 1 (ICAM-1) increased 12-fold more, programmed death ligand 1 (PD-L1) increased 1.4-fold more, and indoleamine 2,3 dioxygenase (IDO) increased 2-fold more with IFNγ/TNFα pre-licensing than IFNγ alone. Both cytokine stimulation conditions resulted in a 1.2-fold decrease in T-cell proliferation. Gland structure and salivary flow are preserved in irradiated mice treated with MSC(SG) pre-licensed with IFNγ/TNFα. B) proposed mechanism of MSC action. R-Spondin 3 and Wnt2b generated by MSC(SG) promote epithelial regeneration after damage from radiation. Radiation also creates a pro-inflammatory local environment with increased dual positive T cells. MSC(SG) might protect local epithelial through optimizing the local inflammatory milieu like protecting macrophages that are important for tissue repair. McCoy, S. (2025) https://BioRender.com/o01d792 . Created in https://BioRender.com .

    Journal: Regenerative Therapy

    Article Title: IFNγ and TNFα optimize salivary gland mesenchymal stromal cells: an alternative to marrow- and adipose-MSCs for radiation xerostomia

    doi: 10.1016/j.reth.2025.11.004

    Figure Lengend Snippet: MSC(SG), particularly after cytokine pre-licensing with IFNγ and TNFα, are a feasible and enhanced MSC source for treatment of radiation-induced xerostomia. Bulk RNA sequencing of MSC(BM), MSC(AD), and MSC(SG) revealed that they shared 85 % of transcripts. Key differences included extracellular matrix production and response to cytokines in MSC(SG). Regardless of MSC source, dual stimulation of MSCs with IFNγ and TNFα produced an average of more than a 20-fold increase in R-Spondin 3 compared to vehicle conditions. Additionally, IFNγ and TNFα pre-licensing optimized immunomodulatory marker expression more than IFNγ alone. Intercellular adhesion molecule 1 (ICAM-1) increased 12-fold more, programmed death ligand 1 (PD-L1) increased 1.4-fold more, and indoleamine 2,3 dioxygenase (IDO) increased 2-fold more with IFNγ/TNFα pre-licensing than IFNγ alone. Both cytokine stimulation conditions resulted in a 1.2-fold decrease in T-cell proliferation. Gland structure and salivary flow are preserved in irradiated mice treated with MSC(SG) pre-licensed with IFNγ/TNFα. B) proposed mechanism of MSC action. R-Spondin 3 and Wnt2b generated by MSC(SG) promote epithelial regeneration after damage from radiation. Radiation also creates a pro-inflammatory local environment with increased dual positive T cells. MSC(SG) might protect local epithelial through optimizing the local inflammatory milieu like protecting macrophages that are important for tissue repair. McCoy, S. (2025) https://BioRender.com/o01d792 . Created in https://BioRender.com .

    Article Snippet: After 48 h of culture, the conditioned media was used for ELISA per the manufacturer's recommendations (GDNF [Innovative Research Novi MI], RSPO1 [CUSABIO, Houston, TX], RSPO3 [Innovative Research], Wnt1 [CUSABIO], Wnt2b [CUSABIO], Wnt3a [CUSABIO], Wnt4 [Raybiotech, Norcross, GA], Wnt5a [CUSABIO]) with dilutions described in the Supplemental Methods.

    Techniques: RNA Sequencing, Produced, Marker, Expressing, Irradiation, Generated