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MedChemExpress migration inhibitor factor mif antagonist iso 1
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Migration Inhibitor Factor Mif Antagonist Iso 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mif+antagonist/bio_rxiv__64898__2026__02__10__705129-256-2-8?v=MedChemExpress
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MedChemExpress mif antagonist
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Mif Antagonist, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Millipore mif antagonist iii, 4-ipp
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Mif Antagonist Iii, 4 Ipp, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress mif antagonist 4 iodo 6 phenylpyrimidine
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Mif Antagonist 4 Iodo 6 Phenylpyrimidine, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mif antagonist 4 iodo 6 phenylpyrimidine - by Bioz Stars, 2026-07
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Millipore mif antagonist (iso-1, #475837)
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Mif Antagonist (Iso 1, #475837), supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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mif antagonist (iso-1, #475837) - by Bioz Stars, 2026-07
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Millipore mif antagonist iso-1
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Mif Antagonist Iso 1, supplied by Millipore, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/mif+antagonist/pm33465053-394-26-29?v=Millipore
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Amano Inc mif antagonist of (s, r) -3- (4- hydroxyphenyl)-4, 5-dihydro-5-isoxazole acetic acid methyl ester (iso-1)
A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter <t>region,</t> <t>ISO-1</t> is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).
Mif Antagonist Of (S, R) 3 (4 Hydroxyphenyl) 4, 5 Dihydro 5 Isoxazole Acetic Acid Methyl Ester (Iso 1), supplied by Amano Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).

Journal: bioRxiv

Article Title: Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

doi: 10.64898/2026.02.10.705129

Figure Lengend Snippet: A) Schematic depicting BulkSignalR pipeline which uses known ligand-receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown to be capable of receiving senescence signals and becoming SA β-gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) ( , S3B). C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (grey) and BrdU (red) treated cell lines (n=3 replicates). D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO-1 is a MIF antagonist, ACT-1004-1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data was analyzed by two-way ANOVA with Tukey’s multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, ** p<0.01, *** p<0.001).

Article Snippet: Treatment with migration inhibitor factor (MIF) antagonist ISO-1 (MedChemExpress, Catalog No. HY-16692) ( ) was utilized to prevent MIF-associated communication between senescence inducers and receiving cells.

Techniques: Activation Assay, RNA sequencing, Expressing, Standard Deviation

A) CCK8 viability assay in astrocytes showing normalized percent cell survival following treatment with DMSO control (grey) or DMSO + Bindarit (pink), DMSO + ISO-1 (blue), DMSO + ACT-1004-1239 (orange), or DMSO + Sitagliptin (green) at various concentrations (n=3 replicates). B) CCK8 viability assay in astrocytes showing normalized percent cell survival following treatment with 100 µM BrdU (red) or BrdU + Bindarit (pink), BrdU + ISO-1 (blue), BrdU + ACT-1004-1239 (orange), or BrdU + Sitagliptin (green) at various concentrations (n=3 replicates). C) CCK8 viability assay in microglia showing normalized percent cell survival following treatment with DMSO control (grey) or DMSO + Bindarit (pink), DMSO + ISO-1 (blue), DMSO + ACT-1004-1239 (orange), or DMSO + Sitagliptin (green) at various concentrations (n=3 replicates). D) CCK8 viability assay in microglia showing normalized percent cell survival following treatment with 100 µM BrdU (red) or BrdU + Bindarit (pink), BrdU + ISO-1 (blue), BrdU + ACT-1004-1239 (orange), or BrdU + Sitagliptin (green) at various concentrations (n=3 replicates). Data analyzed by one-way ANOVA with Dunnett’s correction for multiple comparisons (A-D). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, * p<0.05, ** p<0.01, *** p<0.001).

Journal: bioRxiv

Article Title: Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

doi: 10.64898/2026.02.10.705129

Figure Lengend Snippet: A) CCK8 viability assay in astrocytes showing normalized percent cell survival following treatment with DMSO control (grey) or DMSO + Bindarit (pink), DMSO + ISO-1 (blue), DMSO + ACT-1004-1239 (orange), or DMSO + Sitagliptin (green) at various concentrations (n=3 replicates). B) CCK8 viability assay in astrocytes showing normalized percent cell survival following treatment with 100 µM BrdU (red) or BrdU + Bindarit (pink), BrdU + ISO-1 (blue), BrdU + ACT-1004-1239 (orange), or BrdU + Sitagliptin (green) at various concentrations (n=3 replicates). C) CCK8 viability assay in microglia showing normalized percent cell survival following treatment with DMSO control (grey) or DMSO + Bindarit (pink), DMSO + ISO-1 (blue), DMSO + ACT-1004-1239 (orange), or DMSO + Sitagliptin (green) at various concentrations (n=3 replicates). D) CCK8 viability assay in microglia showing normalized percent cell survival following treatment with 100 µM BrdU (red) or BrdU + Bindarit (pink), BrdU + ISO-1 (blue), BrdU + ACT-1004-1239 (orange), or BrdU + Sitagliptin (green) at various concentrations (n=3 replicates). Data analyzed by one-way ANOVA with Dunnett’s correction for multiple comparisons (A-D). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, * p<0.05, ** p<0.01, *** p<0.001).

Article Snippet: Treatment with migration inhibitor factor (MIF) antagonist ISO-1 (MedChemExpress, Catalog No. HY-16692) ( ) was utilized to prevent MIF-associated communication between senescence inducers and receiving cells.

Techniques: Viability Assay, Control, Standard Deviation

A) Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with 100 µM BrdU (red) along with 200 µM Bindarit (pink), 50 µM ISO-1 (blue), 200 µM ACT-1004-1239 (orange), or 2 µM Sitagliptin (green) (n=6 replicates). B) Quantification of percentage of SA β-gal positive microglia following 7-day treatment with 100 µM BrdU (red) along with 200 µM Bindarit (pink), 50 µM ISO-1 (blue), 200 µM ACT-1004-1239 (orange), or 2 µM Sitagliptin (green) (n=6 replicates). C) Timeline showing treatment with DMSO + Bindarit CM or BrdU + Bindarit CM for 7 days. Timeline showing treatment with DMSO or 100 µM BrdU along with SASP inhibitors (ISO-1, ACT-1004-1239, or Sitagliptin) for 7 days. Features of senescence were analyzed 8 days after the initial plating of cells (created with BioRender). D) Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO + Bindarit CM from astrocytes (grey), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (grey), or BrdU CM from astrocytes + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from astrocytes + Bindarit (grey) or BrdU CM from astrocytes + Bindarit (red) (n=4 replicates). E) Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO + Bindarit CM from microglia (grey), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (grey), or BrdU CM from microglia + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from microglia + Bindarit (grey) or BrdU CM from microglia + Bindarit (red) (n=4 replicates). F) Quantification of percentage of SA β-gal positive microglia following 7-day treatment with DMSO + Bindarit CM from microglia (grey), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (grey), or BrdU CM from microglia + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from microglia + Bindarit (grey) or BrdU CM from microglia + Bindarit (red) (n=4 replicates). G) Quantification of percentage of SA β-gal positive microglia following 7-day treatment with DMSO + Bindarit CM from astrocytes (grey), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (grey), or BrdU CM from astrocytes + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from astrocytes + Bindarit (grey) or BrdU CM from astrocytes + Bindarit (red) (n=4 replicates). Data analyzed by unpaired t-test (A-B) and two-way ANOVA with Tukey’s or Šídák’s multiple comparisons test (D-G). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, * p<0.05, ** p<0.01, *** p<0.001).

Journal: bioRxiv

Article Title: Characterizing the SASP-Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

doi: 10.64898/2026.02.10.705129

Figure Lengend Snippet: A) Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with 100 µM BrdU (red) along with 200 µM Bindarit (pink), 50 µM ISO-1 (blue), 200 µM ACT-1004-1239 (orange), or 2 µM Sitagliptin (green) (n=6 replicates). B) Quantification of percentage of SA β-gal positive microglia following 7-day treatment with 100 µM BrdU (red) along with 200 µM Bindarit (pink), 50 µM ISO-1 (blue), 200 µM ACT-1004-1239 (orange), or 2 µM Sitagliptin (green) (n=6 replicates). C) Timeline showing treatment with DMSO + Bindarit CM or BrdU + Bindarit CM for 7 days. Timeline showing treatment with DMSO or 100 µM BrdU along with SASP inhibitors (ISO-1, ACT-1004-1239, or Sitagliptin) for 7 days. Features of senescence were analyzed 8 days after the initial plating of cells (created with BioRender). D) Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO + Bindarit CM from astrocytes (grey), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (grey), or BrdU CM from astrocytes + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from astrocytes + Bindarit (grey) or BrdU CM from astrocytes + Bindarit (red) (n=4 replicates). E) Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO + Bindarit CM from microglia (grey), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (grey), or BrdU CM from microglia + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from microglia + Bindarit (grey) or BrdU CM from microglia + Bindarit (red) (n=4 replicates). F) Quantification of percentage of SA β-gal positive microglia following 7-day treatment with DMSO + Bindarit CM from microglia (grey), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (grey), or BrdU CM from microglia + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from microglia + Bindarit (grey) or BrdU CM from microglia + Bindarit (red) (n=4 replicates). G) Quantification of percentage of SA β-gal positive microglia following 7-day treatment with DMSO + Bindarit CM from astrocytes (grey), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (grey), or BrdU CM from astrocytes + SASP inhibitor (red) (n=4 replicates). Quantification of percentage of SA β-gal positive astrocytes following 7-day treatment with DMSO CM from astrocytes + Bindarit (grey) or BrdU CM from astrocytes + Bindarit (red) (n=4 replicates). Data analyzed by unpaired t-test (A-B) and two-way ANOVA with Tukey’s or Šídák’s multiple comparisons test (D-G). All graphs show mean with error bars depicting standard deviation (ns, p>0.05, * p<0.05, ** p<0.01, *** p<0.001).

Article Snippet: Treatment with migration inhibitor factor (MIF) antagonist ISO-1 (MedChemExpress, Catalog No. HY-16692) ( ) was utilized to prevent MIF-associated communication between senescence inducers and receiving cells.

Techniques: Standard Deviation