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wnt β catenin pathway  (MedChemExpress)


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    MedChemExpress wnt β catenin pathway
    Effect of SOX10 knockdown and overexpression <t>on</t> <t>classical</t> <t>Wnt/β-catenin</t> pathway-related protein expression in TNBC cell lines. Protein expression of C-myc, CyclinD1, WNT1, phospho-GSK-3β (Ser9), and nuclear β-catenin was detected by Western blot analysis, with band gray values normalized to GAPDH (total protein) or Lamin B1 (nuclear protein, for β-catenin). (A) Protein expression and quantification in MDA-MB-453 cells. (B) Protein expression and quantification in HCC1937 cells. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using unpaired two-tailed Student’s t-test for two-group comparisons. siSOX10 vs. siNC, ** P < 0.01; SOX10-OEvs. NC, ## P < 0.01. && indicates P<0.01; $$ indicates P<0.01 for statistical comparisons.
    Wnt β Catenin Pathway, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 456 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/%CE%B2+catenin+inhibitor/Laduviglusib/pmc13222828-99-1-11
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    Images

    1) Product Images from "Effects of SOX10 on the proliferative, invasive, migratory, and epithelial–mesenchymal transition abilities of triple-negative breast cancer cells"

    Article Title: Effects of SOX10 on the proliferative, invasive, migratory, and epithelial–mesenchymal transition abilities of triple-negative breast cancer cells

    Journal: Frontiers in Oncology

    doi: 10.3389/fonc.2026.1769833

    Effect of SOX10 knockdown and overexpression on classical Wnt/β-catenin pathway-related protein expression in TNBC cell lines. Protein expression of C-myc, CyclinD1, WNT1, phospho-GSK-3β (Ser9), and nuclear β-catenin was detected by Western blot analysis, with band gray values normalized to GAPDH (total protein) or Lamin B1 (nuclear protein, for β-catenin). (A) Protein expression and quantification in MDA-MB-453 cells. (B) Protein expression and quantification in HCC1937 cells. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using unpaired two-tailed Student’s t-test for two-group comparisons. siSOX10 vs. siNC, ** P < 0.01; SOX10-OEvs. NC, ## P < 0.01. && indicates P<0.01; $$ indicates P<0.01 for statistical comparisons.
    Figure Legend Snippet: Effect of SOX10 knockdown and overexpression on classical Wnt/β-catenin pathway-related protein expression in TNBC cell lines. Protein expression of C-myc, CyclinD1, WNT1, phospho-GSK-3β (Ser9), and nuclear β-catenin was detected by Western blot analysis, with band gray values normalized to GAPDH (total protein) or Lamin B1 (nuclear protein, for β-catenin). (A) Protein expression and quantification in MDA-MB-453 cells. (B) Protein expression and quantification in HCC1937 cells. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using unpaired two-tailed Student’s t-test for two-group comparisons. siSOX10 vs. siNC, ** P < 0.01; SOX10-OEvs. NC, ## P < 0.01. && indicates P<0.01; $$ indicates P<0.01 for statistical comparisons.

    Techniques Used: Knockdown, Over Expression, Expressing, Western Blot, Two Tailed Test

    SOX10 promotes EMT in MDA-MB-453 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 MDA-MB-453 cells treated with a Wnt activator, and SOX10-overexpressing MDA-MB-453 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with MDA-MB-453+siNC, * P < 0.05, ** P < 0.01; compared with MDA-MB-453+siSOX10, # P < 0.05, ## P < 0.01; compared with MDA-MB-453+NC.
    Figure Legend Snippet: SOX10 promotes EMT in MDA-MB-453 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 MDA-MB-453 cells treated with a Wnt activator, and SOX10-overexpressing MDA-MB-453 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with MDA-MB-453+siNC, * P < 0.05, ** P < 0.01; compared with MDA-MB-453+siSOX10, # P < 0.05, ## P < 0.01; compared with MDA-MB-453+NC.

    Techniques Used: Expressing, Western Blot

    SOX10 promotes EMT in HCC1937 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 HCC1937 cells treated with a Wnt activator, and SOX10-overexpressing HCC1937 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with HCC1937+siNC, ** P < 0.01; compared with HCC1937+siSOX10, ## P < 0.01; compared with HCC1937+NC.
    Figure Legend Snippet: SOX10 promotes EMT in HCC1937 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 HCC1937 cells treated with a Wnt activator, and SOX10-overexpressing HCC1937 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with HCC1937+siNC, ** P < 0.01; compared with HCC1937+siSOX10, ## P < 0.01; compared with HCC1937+NC.

    Techniques Used: Expressing, Western Blot

    Related Articles

    In Vitro:

    Article Title: The promoting roles of GLP1R and GIPR in stemness maintenance and multiple lineage-specific differentiation of PDLSCs
    Article Snippet: .. The in vitro treatment conditions for the small-molecule compound were as follows: GLP1RA semaglutide acetate (10 nM, 24 h), GIPRA (Pro3) GIP (0.5 nM, 24 h), GLP-1R/GIPR agonist-1 (10 nM, 24 h) also termed as 2GRA in this study, BGM0504 (2 nM, 24 h, BrightGene Pharmaceutical Co., Ltd., China) [ ], CREB inhibitor 666-15 (1 μM, 2 h, HY-101120, MCE), Akt inhibitor MK-2206 (5 μM, 24 h, HY-108232, MCE), ERK1/2 inhibitor SCH772984 (0.5 μM, 24 h, HY-50846, MCE), β-catenin inhibitor IN-3 (5 μM, 24 h, HY-147007, MCE), STAT3-IN-14 (5 μM, 2 h, HY-N10472, MCE). .. PDLSCs were induced to differentiate into osteogenic (HUXXC-90021, OriCell, China), adipogenic (HUXXC-90031, OriCell), and chondrogenic (HUXXC-90041, OriCell) lineages using commercial differentiation kits according to the manufacturer’s protocols.

    Article Title: The promoting roles of GLP1R and GIPR in stemness maintenance and multiple lineage-specific differentiation of PDLSCs.
    Article Snippet: .. The in vitro treatment conditions for the small-molecule compound were as follows: GLP1RA semaglutide acetate (10 nM, 24 h), GIPRA (Pro3) GIP (0.5 nM, 24 h), GLP1R/GIPR agonist-1 (10 nM, 24 h) also termed as 2GRA in this study, BGM0504 (2 nM, 24 h, BrightGene Pharmaceutical Co., Ltd., China) [13], CREB inhibitor 666-15 (1 μM, 2 h, HY-101120, MCE), Akt inhibitor MK-2206 (5 μM, 24 h, HY-108232, MCE), ERK1/2 inhibitor SCH772984 (0.5 μM, 24 h, HY-50846, MCE), β-catenin inhibitor IN-3 (5 μM, 24 h, HY-147007, MCE), STAT3-IN-14 (5 μM, 2 h, HY-N10472, MCE). .. PDLSCs were induced to differentiate into osteogenic (HUXXC-90021, OriCell, China), adipogenic (HUXXC-90031, OriCell), and chondrogenic (HUXXC-90041, OriCell) lineages using commercial differentiation kits according to the manufacturer’s protocols.

    SPR Assay:

    Article Title: Aucubin inhibits the activity of lung cancer stem-like cells by targeting degradation of β-catenin.
    Article Snippet: Objectives: To investigate the antitumor effects of aucubin (AC) in non-small cell lung cancer (NSCLC) and uncover its plausible mechanism against lung cancer stem-like cells (LCSCs).. Methods: In vitro experiments included MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, a reagent commonly used for cell viability assay) and colony formation assays to assess anti-proliferative effects on A549 and NCI-H1975 lung cancer cell lines, wound healing and Transwell invasion assays to evaluate inhibition of cell migration and invasion, tumorsphere-formation experiments to detect changes in NSCLC cell stemness, as well as Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR) analyses to measure the expression of LCSC markers (CD44, CD133, Oct4, and Nanog).. In vivo experiments were conducted to observe the impact of AC on NSCLC metastasis and mouse survival rates.

    Binding Assay:

    Article Title: Aucubin inhibits the activity of lung cancer stem-like cells by targeting degradation of β-catenin.
    Article Snippet: Objectives: To investigate the antitumor effects of aucubin (AC) in non-small cell lung cancer (NSCLC) and uncover its plausible mechanism against lung cancer stem-like cells (LCSCs).. Methods: In vitro experiments included MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, a reagent commonly used for cell viability assay) and colony formation assays to assess anti-proliferative effects on A549 and NCI-H1975 lung cancer cell lines, wound healing and Transwell invasion assays to evaluate inhibition of cell migration and invasion, tumorsphere-formation experiments to detect changes in NSCLC cell stemness, as well as Western blot and quantitative reverse transcription polymerase chain reaction (qRT-PCR) analyses to measure the expression of LCSC markers (CD44, CD133, Oct4, and Nanog).. In vivo experiments were conducted to observe the impact of AC on NSCLC metastasis and mouse survival rates.

    Inhibition:

    Article Title: MiR-488-3p facilitates wound healing through CYP1B1-mediated Wnt/β-catenin signaling pathway by targeting MeCP2.
    Article Snippet: Human skin fibroblasts (HSF), keratinocytes (HaCaT), and human umbilical vein endothelial cells (HUVECs), purchased from ATCC (Manassas, VA, USA), were cultured in DMEM (Gibco, Carlsbad, CA, USA) containing 10% FBS (Gibco) at 37°C with 5% CO2. .. For β-catenin inhibition, HSF cells and HUVECs were treated with a β-catenin inhibitor (JW 55, 5 μM) (Medchemexpress, Shanghai, China) for 24 h. For CYP1B1 inhibition, HSF cells and HUVECs were treated with a CYP1B1 inhibitor (CYP1B1-IN-1, 10 μM; Medchemexpress) for 24 h. .. GenePharma (Shanghai, China) provided the overexpression plasmid of MeCP2 (oe-MeCP2), the short hairpin RNA of CYP1B1 (sh-CYP1B1), the mimics or inhibitors of miR-488-3p, and the negative controls, which were transfected into cells with LipofectamineTM 3000 (Invitrogen, Carlsbad, CA, USA).

    Article Title: MiR ‐488‐3p facilitates wound healing through CYP1B1 ‐mediated Wnt/β‐catenin signaling pathway by targeting MeCP2
    Article Snippet: Human skin fibroblasts (HSF), keratinocytes (HaCaT), and human umbilical vein endothelial cells (HUVECs), purchased from ATCC (Manassas, VA, USA), were cultured in DMEM (Gibco, Carlsbad, CA, USA) containing 10% FBS (Gibco) at 37°C with 5% CO 2 . .. For β‐catenin inhibition, HSF cells and HUVECs were treated with a β‐catenin inhibitor (JW 55, 5 μM) (Medchemexpress, Shanghai, China) for 24 h. For CYP1B1 inhibition, HSF cells and HUVECs were treated with a CYP1B1 inhibitor (CYP1B1‐IN‐1, 10 μM; Medchemexpress) for 24 h. .. GenePharma (Shanghai, China) provided the overexpression plasmid of MeCP2 (oe‐MeCP2), the short hairpin RNA of CYP1B1 (sh‐CYP1B1), the mimics or inhibitors of miR‐488‐3p, and the negative controls, which were transfected into cells with LipofectamineTM 3000 (Invitrogen, Carlsbad, CA, USA).



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    Image Search Results


    Effect of SOX10 knockdown and overexpression on classical Wnt/β-catenin pathway-related protein expression in TNBC cell lines. Protein expression of C-myc, CyclinD1, WNT1, phospho-GSK-3β (Ser9), and nuclear β-catenin was detected by Western blot analysis, with band gray values normalized to GAPDH (total protein) or Lamin B1 (nuclear protein, for β-catenin). (A) Protein expression and quantification in MDA-MB-453 cells. (B) Protein expression and quantification in HCC1937 cells. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using unpaired two-tailed Student’s t-test for two-group comparisons. siSOX10 vs. siNC, ** P < 0.01; SOX10-OEvs. NC, ## P < 0.01. && indicates P<0.01; $$ indicates P<0.01 for statistical comparisons.

    Journal: Frontiers in Oncology

    Article Title: Effects of SOX10 on the proliferative, invasive, migratory, and epithelial–mesenchymal transition abilities of triple-negative breast cancer cells

    doi: 10.3389/fonc.2026.1769833

    Figure Lengend Snippet: Effect of SOX10 knockdown and overexpression on classical Wnt/β-catenin pathway-related protein expression in TNBC cell lines. Protein expression of C-myc, CyclinD1, WNT1, phospho-GSK-3β (Ser9), and nuclear β-catenin was detected by Western blot analysis, with band gray values normalized to GAPDH (total protein) or Lamin B1 (nuclear protein, for β-catenin). (A) Protein expression and quantification in MDA-MB-453 cells. (B) Protein expression and quantification in HCC1937 cells. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using unpaired two-tailed Student’s t-test for two-group comparisons. siSOX10 vs. siNC, ** P < 0.01; SOX10-OEvs. NC, ## P < 0.01. && indicates P<0.01; $$ indicates P<0.01 for statistical comparisons.

    Article Snippet: The Wnt/β-catenin pathway was activated using CHIR-99021 (a selective GSK-3β inhibitor; MedChemExpress, Monmouth Junction, New Jersey, United States, Cat. No. HY-10182) at a concentration of 5 μM , and inhibited using XAV939 (a tankyrase 1/2 inhibitor; MedChemExpress, Cat. No. HY-15147) at a concentration of 10 μM ( ).

    Techniques: Knockdown, Over Expression, Expressing, Western Blot, Two Tailed Test

    SOX10 promotes EMT in MDA-MB-453 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 MDA-MB-453 cells treated with a Wnt activator, and SOX10-overexpressing MDA-MB-453 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with MDA-MB-453+siNC, * P < 0.05, ** P < 0.01; compared with MDA-MB-453+siSOX10, # P < 0.05, ## P < 0.01; compared with MDA-MB-453+NC.

    Journal: Frontiers in Oncology

    Article Title: Effects of SOX10 on the proliferative, invasive, migratory, and epithelial–mesenchymal transition abilities of triple-negative breast cancer cells

    doi: 10.3389/fonc.2026.1769833

    Figure Lengend Snippet: SOX10 promotes EMT in MDA-MB-453 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 MDA-MB-453 cells treated with a Wnt activator, and SOX10-overexpressing MDA-MB-453 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with MDA-MB-453+siNC, * P < 0.05, ** P < 0.01; compared with MDA-MB-453+siSOX10, # P < 0.05, ## P < 0.01; compared with MDA-MB-453+NC.

    Article Snippet: The Wnt/β-catenin pathway was activated using CHIR-99021 (a selective GSK-3β inhibitor; MedChemExpress, Monmouth Junction, New Jersey, United States, Cat. No. HY-10182) at a concentration of 5 μM , and inhibited using XAV939 (a tankyrase 1/2 inhibitor; MedChemExpress, Cat. No. HY-15147) at a concentration of 10 μM ( ).

    Techniques: Expressing, Western Blot

    SOX10 promotes EMT in HCC1937 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 HCC1937 cells treated with a Wnt activator, and SOX10-overexpressing HCC1937 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with HCC1937+siNC, ** P < 0.01; compared with HCC1937+siSOX10, ## P < 0.01; compared with HCC1937+NC.

    Journal: Frontiers in Oncology

    Article Title: Effects of SOX10 on the proliferative, invasive, migratory, and epithelial–mesenchymal transition abilities of triple-negative breast cancer cells

    doi: 10.3389/fonc.2026.1769833

    Figure Lengend Snippet: SOX10 promotes EMT in HCC1937 cells via activating the classical Wnt/β-catenin signaling pathway. (A) Relative protein expression of Wnt/β-catenin pathway-related factors (WNT1, β-catenin, C-myc, and CyclinD1) in siSOX10 HCC1937 cells treated with a Wnt activator, and SOX10-overexpressing HCC1937 cells treated with a Wnt inhibitor. (B) Relative protein expression of EMT-related markers (E-cadherin, N-cadherin, and Vimentin) in the aforementioned treatment groups. All protein levels were detected by Western blot analysis, with band gray values normalized to GAPDH. All experiments were independently repeated three times (n = 3 independent biological replicates), and representative results are shown. Statistical analysis was performed using one-way ANOVA with Tukey’s post-hoc test for multiple comparisons among groups. Compared with HCC1937+siNC, ** P < 0.01; compared with HCC1937+siSOX10, ## P < 0.01; compared with HCC1937+NC.

    Article Snippet: The Wnt/β-catenin pathway was activated using CHIR-99021 (a selective GSK-3β inhibitor; MedChemExpress, Monmouth Junction, New Jersey, United States, Cat. No. HY-10182) at a concentration of 5 μM , and inhibited using XAV939 (a tankyrase 1/2 inhibitor; MedChemExpress, Cat. No. HY-15147) at a concentration of 10 μM ( ).

    Techniques: Expressing, Western Blot

    Isolated Wnt-responsive cells were cultured in vitro and treated with the Wnt pathway inhibitor XAV-939 (1 μM or 5 μM), the Foxm1 inhibitor RCM-1 (4 μM or 20 μM), or the Wnt agonist Wnt agonist 1 (0.2 nM or 1 nM). Cell proliferation was quantified by measuring total cell number after treatment. Pharmacological inhibition of canonical Wnt signaling using XAV-939 significantly reduced cell expansion compared with control cultures. Similarly, inhibition of Foxm1 using RCM-1 markedly suppressed proliferation. In contrast, activation of canonical Wnt signaling by Wnt agonist 1 increased cell numbers relative to controls. These findings support a cooperative role for canonical Wnt signaling and Foxm1 in promoting proliferative capacity of Wnt-responsive cells in vitro . Bars represent mean ± s.d. Each dot represents one biologically independent sample. Statistical significance was determined by one-way ANOVA followed by multiple comparisons testing. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Journal: bioRxiv

    Article Title: A Wnt-responsive fibrocartilage progenitor system coordinates postnatal mandibular condylar cartilage growth

    doi: 10.64898/2026.03.25.714159

    Figure Lengend Snippet: Isolated Wnt-responsive cells were cultured in vitro and treated with the Wnt pathway inhibitor XAV-939 (1 μM or 5 μM), the Foxm1 inhibitor RCM-1 (4 μM or 20 μM), or the Wnt agonist Wnt agonist 1 (0.2 nM or 1 nM). Cell proliferation was quantified by measuring total cell number after treatment. Pharmacological inhibition of canonical Wnt signaling using XAV-939 significantly reduced cell expansion compared with control cultures. Similarly, inhibition of Foxm1 using RCM-1 markedly suppressed proliferation. In contrast, activation of canonical Wnt signaling by Wnt agonist 1 increased cell numbers relative to controls. These findings support a cooperative role for canonical Wnt signaling and Foxm1 in promoting proliferative capacity of Wnt-responsive cells in vitro . Bars represent mean ± s.d. Each dot represents one biologically independent sample. Statistical significance was determined by one-way ANOVA followed by multiple comparisons testing. *P < 0.05; **P < 0.01; ***P < 0.001; ****P < 0.0001.

    Article Snippet: Pharmacological treatments were performed using the Foxm1 inhibitor RCM-1, the β-catenin inhibitor XAV-939, or a canonical Wnt pathway activator (Wnt agonist 1) (all from Selleck Chemicals, Japan).

    Techniques: Isolation, Cell Culture, In Vitro, Inhibition, Control, Activation Assay

    β-catenin inhibition attenuates endothelial exosome-induced β-catenin activation in HAVSMCs. ( A , C ) Representative Western blot images showing non-phosphorylated (active) β-catenin protein expression in human aortic vascular smooth muscle cells (HAVSMCs) treated with endothelial cell-derived exosomes (EC-EXOs) obtained from TNFα-, TGFβ-, or TMAO-stimulated endothelial cells, in the presence or absence of the β-catenin transcriptional inhibitor ICG-001 for 8 days. β-actin was used as a loading control. ( B , D ) Quantitative densitometric analysis demonstrates a significant increase in β-catenin protein levels following EC-EXO treatment, which was markedly reduced upon β-catenin inhibition with ICG-001. Protein expression levels were normalized to β-actin and expressed as fold change relative to vehicle-treated controls. Data are presented as mean ± standard deviation (SD) from three independent biological replicates. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test to assess differences between EC-EXO treatment groups and the effect of β-catenin inhibition. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Journal: Cells

    Article Title: TMAO-Triggered Endothelial–Mesenchymal Transition and Microvesicle Release as Mediators of Vascular Smooth Muscle Cell Osteogenic Differentiation and Vascular Calcification

    doi: 10.3390/cells15050466

    Figure Lengend Snippet: β-catenin inhibition attenuates endothelial exosome-induced β-catenin activation in HAVSMCs. ( A , C ) Representative Western blot images showing non-phosphorylated (active) β-catenin protein expression in human aortic vascular smooth muscle cells (HAVSMCs) treated with endothelial cell-derived exosomes (EC-EXOs) obtained from TNFα-, TGFβ-, or TMAO-stimulated endothelial cells, in the presence or absence of the β-catenin transcriptional inhibitor ICG-001 for 8 days. β-actin was used as a loading control. ( B , D ) Quantitative densitometric analysis demonstrates a significant increase in β-catenin protein levels following EC-EXO treatment, which was markedly reduced upon β-catenin inhibition with ICG-001. Protein expression levels were normalized to β-actin and expressed as fold change relative to vehicle-treated controls. Data are presented as mean ± standard deviation (SD) from three independent biological replicates. Statistical significance was determined by one-way ANOVA followed by Tukey’s post hoc test to assess differences between EC-EXO treatment groups and the effect of β-catenin inhibition. * p < 0.05, ** p < 0.01, *** p < 0.001.

    Article Snippet: To determine the requirement of Wnt/β-catenin signaling in endothelial exosome-induced osteogenic reprogramming, HAVSMCs were treated with the selective β-catenin/CBP transcriptional inhibitor ICG-001 (TargetMol).

    Techniques: Inhibition, Activation Assay, Western Blot, Expressing, Derivative Assay, Control, Standard Deviation

    β-catenin inhibition suppresses endothelial exosome-induced osteogenic gene expression in HAVSMCs. ( A – E ) Quantitative real-time PCR analysis of osteogenic gene expression in HAVSMCs treated with endothelial cell-derived exosomes (EC-EXOs) from TNFα-, TGFβ-, or TMAO-stimulated endothelial cells, in the presence of the β-catenin inhibitor ICG-001. Relative mRNA expression levels of ( A ) SM22A, ( B ) αSMA, ( C ) RUNX2, ( D ) osteopontin (OPN), and ( E ) tissue-nonspecific alkaline phosphatase (TNAP) were normalized to housekeeping genes and expressed relative to vehicle-treated control cells (0.1% v / v DMSO). EC-EXO co-treatment with ICG-001 significantly attenuated the expression of RUNX2, OPN, and TNAP, indicating that β-catenin signaling is required for endothelial exosome-induced osteogenic reprogramming of HAVSMCs. Data are presented as mean ± SD from three independent biological replicates. Statistical significance was assessed using one-way ANOVA, followed by post-hoc analysis. * p < 0.05, ** p < 0.01, *** p < 0.001, vs. CTL vehicle.

    Journal: Cells

    Article Title: TMAO-Triggered Endothelial–Mesenchymal Transition and Microvesicle Release as Mediators of Vascular Smooth Muscle Cell Osteogenic Differentiation and Vascular Calcification

    doi: 10.3390/cells15050466

    Figure Lengend Snippet: β-catenin inhibition suppresses endothelial exosome-induced osteogenic gene expression in HAVSMCs. ( A – E ) Quantitative real-time PCR analysis of osteogenic gene expression in HAVSMCs treated with endothelial cell-derived exosomes (EC-EXOs) from TNFα-, TGFβ-, or TMAO-stimulated endothelial cells, in the presence of the β-catenin inhibitor ICG-001. Relative mRNA expression levels of ( A ) SM22A, ( B ) αSMA, ( C ) RUNX2, ( D ) osteopontin (OPN), and ( E ) tissue-nonspecific alkaline phosphatase (TNAP) were normalized to housekeeping genes and expressed relative to vehicle-treated control cells (0.1% v / v DMSO). EC-EXO co-treatment with ICG-001 significantly attenuated the expression of RUNX2, OPN, and TNAP, indicating that β-catenin signaling is required for endothelial exosome-induced osteogenic reprogramming of HAVSMCs. Data are presented as mean ± SD from three independent biological replicates. Statistical significance was assessed using one-way ANOVA, followed by post-hoc analysis. * p < 0.05, ** p < 0.01, *** p < 0.001, vs. CTL vehicle.

    Article Snippet: To determine the requirement of Wnt/β-catenin signaling in endothelial exosome-induced osteogenic reprogramming, HAVSMCs were treated with the selective β-catenin/CBP transcriptional inhibitor ICG-001 (TargetMol).

    Techniques: Inhibition, Gene Expression, Real-time Polymerase Chain Reaction, Derivative Assay, Expressing, Control