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Orf Expression Clone For Csf1, supplied by Genecopoeia, 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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Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic <t>(CSF1)</t> macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.
Csf1 M Csf, supplied by Miltenyi Biotec, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic <t>(CSF1)</t> macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.
Gene Exp Csf1 Hs00174164 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic <t>(CSF1)</t> macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.
Gene Exp Csf1 Mm00432686 M1, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic <t>(CSF1)</t> macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.
Csf1 Protein Levels, supplied by Boster Bio, 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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Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic <t>(CSF1)</t> macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.
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Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic (CSF1) macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.

Journal: Scientific Reports

Article Title: Suppression of CSF2RA macrophage polarisation impacts pathological cardiac remodelling in mice

doi: 10.1038/s41598-025-33936-1

Figure Lengend Snippet: Loss of CSF2 macrophage polarisation promotes CXCL10 expression and CXCR3-induced cardiac fibroblast dedifferentiation, while CSF2-macrophage CTSZ degrades CXCL10. Validation of CTSZ and CXCL10 expression in (A) + CSF2 or -CSF2 macrophage secretome ( n = 7 and 4), and (B) cell lysates ( n = 7 and 8). Quantification and representative images of α-SMA assessed through immunocytochemistry (red in panel C, green in panel F): (C) supplementing CXCL10 protein (50 ng/mL) in the + CSF2 secretome ( n = 10); (D) effect of CXCL10 protein (50 ng/mL) and AMG487 (1 µM), a CXCR3 inhibitor, on naïve cardiac fibroblasts ( n = 4); (E) effect of CXCR3 inhibition, through AMG487 (1 µM) on -CSF2 secretome effect on cardiac fibroblast α-SMA expression ( n = 4); (F) inhibition of CTSZ protein (4 µg/mL) in the + CSF2 secretome ( n = 6, IgG n = 4); (G) effect of CTSZ protein (6 ng/mL) ( n = 3) or (H) inhibition of CTSZ protein (4 µg/mL) on naïve cardiac fibroblasts ( n = 3); (I) supplementing CTSZ protein (6 ng/mL) in macrophage secretome ( n = 4). (J) CTSZ cleavage of CXCL10 protein ( n = 4) and (K) effect on cardiac fibroblast α-SMA expression, assessed through immunocytochemistry ( n = 5). (L) Proposed CTSZ/CXCL10-mediated mechanism in crosstalk between pro-inflammatory (CSF2) or pro-fibrotic (CSF1) macrophages and cardiac fibroblasts; generated using bioRender ( https://www.biorender.com ). Statistical significance is reported as * P < 0.05, ** P < 0.01, or *** P < 0.001, using paired Students t-test to panels A, B, and J; ordinary one-way ANOVA, to panels C-F, and I, or repeated measures one-way ANOVA, to panel K, with Tukey’s multiple comparisons post-hoc. Scale bar represents 200 µM and is applicable to panels C and F.

Article Snippet: Monocytes were cultured for 7 days with the appropriate CSFs: 40 ng/mL CSF1 (M-CSF) (catalogue number 130-096-491, Miltenyi Biotec) or 20 ng/mL CSF1 (M-CSF) and 20 ng/mL CSF2 (GM-CSF) (catalogue number 130-095-372, Miltenyi Biotec), to differentiate into CSF1 (M-) or CSF2 (GM-) macrophage subsets, respectively.

Techniques: Expressing, Biomarker Discovery, Immunocytochemistry, Inhibition, Generated