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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01
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Image Search Results


EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig.  and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01

Journal: Molecular Biomedicine

Article Title: EZH2 coordinates inflammatory and pain-associated pathways across joint compartments in osteoarthritis

doi: 10.1186/s43556-026-00643-w

Figure Lengend Snippet: EZH2 inhibition reduced the inflammatory phenotype of macrophages during OA. Macrophage differentiation and M1-like polarization were induced from the THP-1 monocytic cell line ( a ) or from human bone marrow-derived cells isolated from OA patients ( b ) in the presence or absence of EPZ-6438. The expression of pro-inflammatory markers (IL-1β, IL-6 and CXCL1) was analyzed by RT-qPCR. Experiments using THP-1 cells were independently repeated at least three times. Experiments using human bone marrow-derived cells were performed using biological replicates from independent OA patients. Data are presented as mean ± SEM. *: p -value < 0.05; **: p -value < 0.01; ***: p -value < 0.001. Spleens from OA mice described in Fig. and treated with vehicle or EPZ-6438 were collected and analyzed by flow cytometry. Cells were stained for macrophage-associated markers ( c ). Samples were acquired using a FACSVerse flow cytometer and analyzed with FlowJo 7.6.5 software. Results are presented as median ± interquartile range (n = 8 mice). *: p -value < 0.05; **: p -value < 0.01

Article Snippet: The following antibodies were used for immune cell characterization: CD11b (REA592 VioBlue, 130–113–810, Miltenyi Biotec), F4/80 (REA126 PE-Vio770, 130–118–459, Miltenyi Biotec), CD80 (REA983 APC-Vio770, 130–116–463, Miltenyi Biotec), CD86 (REA1190 PE, 130–122–129, Miltenyi Biotec), MHC-II (REA813 FITC, 130–112–386, Miltenyi Biotec), CD38 (REA616 PerCP-Vio700, 130–109–260, Miltenyi Biotec), and iNOS (REA982 APC, 130–116–423, Miltenyi Biotec).

Techniques: Inhibition, Derivative Assay, Isolation, Expressing, Quantitative RT-PCR, Flow Cytometry, Staining, Software