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MedChemExpress hy p7265
<t>CCL-18</t> <t>may</t> be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).
Hy P7265, 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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TargetMol recombinant rat ccl3 protein
<t>CCL-18</t> <t>may</t> be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).
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Santa Cruz Biotechnology sc 374438 rrid ab 10989263
<t>CCL-18</t> <t>may</t> be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).
Sc 374438 Rrid Ab 10989263, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Bio-Techne corporation mouse ccl3/mip-1 alpha antibody
<t>CCL-18</t> <t>may</t> be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).
Mouse Ccl3/Mip 1 Alpha Antibody, supplied by Bio-Techne corporation, 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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Bio-Techne corporation mouse ccl4/mip-1 beta antibody
<t>CCL-18</t> <t>may</t> be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).
Mouse Ccl4/Mip 1 Beta Antibody, supplied by Bio-Techne corporation, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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MedChemExpress human medchemexpress cat
<t>CCL-18</t> <t>may</t> be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).
Human Medchemexpress Cat, 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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MedChemExpress hifs
Human CCL15 promotes the activation, proliferation, and migration of human intestinal fibroblasts. (A) Representative images of Masson's trichrome staining and IHC showing fibrosis levels and hCCL15 expression in stenotic and non‐stenotic intestinal surgical specimens from patients with CD. Scale bar: 500 µm (low magnification) and 100 µm (high magnification). n = 4 patients; 3 fields per zone. (B) Relative CCL15 mRNA abundance in stricture versus non‐stricture regions was quantified by RT‐qPCR. (C) Serum concentrations of hCCL15 in CD patients with or without intestinal strictures were detected using ELISA. (D) Correlation analysis between CCL15 and collagen‐associated genes ( COL1A1, COL6A1, COL3A1 , and FN1 ) in CD intestines. (E) Human intestinal fibroblasts <t>(HIFs)</t> isolated from stenotic regions were treated <t>with</t> <t>recombinant</t> CCL15 (5,10, and 20 ng/mL) for 48 h, and COL1A1 protein levels were then assessed by Western blot. (F–H) HIFs were stimulated with hCCL15 (10 ng/mL) for 48 h. Migration was assessed by wound healing assay (F; Scale bar: 500 µm). α‐SMA and Ki67 immunofluorescence staining was performed to evaluate activation and proliferation, and Ki67+ cells were quantified (G; Scale bar: 100 µm). mRNA levels of ACTA2 , COL1A1 , COL3A1 , COL6A1 , COL6A3 , and FN1 were measured by RT‐qPCR (H). I) Immunofluorescence co‐localization analysis of S100A8/A9 + CCL15 + macrophages and CCR1 + α‐SMA + fibroblasts in intestinal stricture sections from patients with CD. Red arrows indicate S100A8/A9 + CCL15 + macrophages located within 30 µm of the nearest fibroblast; white arrows indicate CCR1 + fibroblasts. Scale bars: 50 µm (low magnification) and 20 µm (high magnification). n = 4 patients; 3 fields per zone. All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
Hifs, 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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3M Co transbond mip
Human CCL15 promotes the activation, proliferation, and migration of human intestinal fibroblasts. (A) Representative images of Masson's trichrome staining and IHC showing fibrosis levels and hCCL15 expression in stenotic and non‐stenotic intestinal surgical specimens from patients with CD. Scale bar: 500 µm (low magnification) and 100 µm (high magnification). n = 4 patients; 3 fields per zone. (B) Relative CCL15 mRNA abundance in stricture versus non‐stricture regions was quantified by RT‐qPCR. (C) Serum concentrations of hCCL15 in CD patients with or without intestinal strictures were detected using ELISA. (D) Correlation analysis between CCL15 and collagen‐associated genes ( COL1A1, COL6A1, COL3A1 , and FN1 ) in CD intestines. (E) Human intestinal fibroblasts <t>(HIFs)</t> isolated from stenotic regions were treated <t>with</t> <t>recombinant</t> CCL15 (5,10, and 20 ng/mL) for 48 h, and COL1A1 protein levels were then assessed by Western blot. (F–H) HIFs were stimulated with hCCL15 (10 ng/mL) for 48 h. Migration was assessed by wound healing assay (F; Scale bar: 500 µm). α‐SMA and Ki67 immunofluorescence staining was performed to evaluate activation and proliferation, and Ki67+ cells were quantified (G; Scale bar: 100 µm). mRNA levels of ACTA2 , COL1A1 , COL3A1 , COL6A1 , COL6A3 , and FN1 were measured by RT‐qPCR (H). I) Immunofluorescence co‐localization analysis of S100A8/A9 + CCL15 + macrophages and CCR1 + α‐SMA + fibroblasts in intestinal stricture sections from patients with CD. Red arrows indicate S100A8/A9 + CCL15 + macrophages located within 30 µm of the nearest fibroblast; white arrows indicate CCR1 + fibroblasts. Scale bars: 50 µm (low magnification) and 20 µm (high magnification). n = 4 patients; 3 fields per zone. All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
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MedChemExpress ccl19
Human CCL15 promotes the activation, proliferation, and migration of human intestinal fibroblasts. (A) Representative images of Masson's trichrome staining and IHC showing fibrosis levels and hCCL15 expression in stenotic and non‐stenotic intestinal surgical specimens from patients with CD. Scale bar: 500 µm (low magnification) and 100 µm (high magnification). n = 4 patients; 3 fields per zone. (B) Relative CCL15 mRNA abundance in stricture versus non‐stricture regions was quantified by RT‐qPCR. (C) Serum concentrations of hCCL15 in CD patients with or without intestinal strictures were detected using ELISA. (D) Correlation analysis between CCL15 and collagen‐associated genes ( COL1A1, COL6A1, COL3A1 , and FN1 ) in CD intestines. (E) Human intestinal fibroblasts <t>(HIFs)</t> isolated from stenotic regions were treated <t>with</t> <t>recombinant</t> CCL15 (5,10, and 20 ng/mL) for 48 h, and COL1A1 protein levels were then assessed by Western blot. (F–H) HIFs were stimulated with hCCL15 (10 ng/mL) for 48 h. Migration was assessed by wound healing assay (F; Scale bar: 500 µm). α‐SMA and Ki67 immunofluorescence staining was performed to evaluate activation and proliferation, and Ki67+ cells were quantified (G; Scale bar: 100 µm). mRNA levels of ACTA2 , COL1A1 , COL3A1 , COL6A1 , COL6A3 , and FN1 were measured by RT‐qPCR (H). I) Immunofluorescence co‐localization analysis of S100A8/A9 + CCL15 + macrophages and CCR1 + α‐SMA + fibroblasts in intestinal stricture sections from patients with CD. Red arrows indicate S100A8/A9 + CCL15 + macrophages located within 30 µm of the nearest fibroblast; white arrows indicate CCR1 + fibroblasts. Scale bars: 50 µm (low magnification) and 20 µm (high magnification). n = 4 patients; 3 fields per zone. All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
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Medicago mip mimif1
Human CCL15 promotes the activation, proliferation, and migration of human intestinal fibroblasts. (A) Representative images of Masson's trichrome staining and IHC showing fibrosis levels and hCCL15 expression in stenotic and non‐stenotic intestinal surgical specimens from patients with CD. Scale bar: 500 µm (low magnification) and 100 µm (high magnification). n = 4 patients; 3 fields per zone. (B) Relative CCL15 mRNA abundance in stricture versus non‐stricture regions was quantified by RT‐qPCR. (C) Serum concentrations of hCCL15 in CD patients with or without intestinal strictures were detected using ELISA. (D) Correlation analysis between CCL15 and collagen‐associated genes ( COL1A1, COL6A1, COL3A1 , and FN1 ) in CD intestines. (E) Human intestinal fibroblasts <t>(HIFs)</t> isolated from stenotic regions were treated <t>with</t> <t>recombinant</t> CCL15 (5,10, and 20 ng/mL) for 48 h, and COL1A1 protein levels were then assessed by Western blot. (F–H) HIFs were stimulated with hCCL15 (10 ng/mL) for 48 h. Migration was assessed by wound healing assay (F; Scale bar: 500 µm). α‐SMA and Ki67 immunofluorescence staining was performed to evaluate activation and proliferation, and Ki67+ cells were quantified (G; Scale bar: 100 µm). mRNA levels of ACTA2 , COL1A1 , COL3A1 , COL6A1 , COL6A3 , and FN1 were measured by RT‐qPCR (H). I) Immunofluorescence co‐localization analysis of S100A8/A9 + CCL15 + macrophages and CCR1 + α‐SMA + fibroblasts in intestinal stricture sections from patients with CD. Red arrows indicate S100A8/A9 + CCL15 + macrophages located within 30 µm of the nearest fibroblast; white arrows indicate CCR1 + fibroblasts. Scale bars: 50 µm (low magnification) and 20 µm (high magnification). n = 4 patients; 3 fields per zone. All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.
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CCL-18 may be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 may be the candidate-mediator of glioma recurrence (A) KEGG enrichment analysis of the 201 DEGs showing that the cytokine-cytokine receptor interaction pathway was the most significantly enriched. (B) Among cytokine-cytokine receptor interaction pathway, CCL-18 was the top one up-regulated DEG. Data were presented as average TPM. (C) Representative IHC staining of CCL-18 in primary and recurrent glioma samples from irradiated patients versus unirradiated patients. Scale bars: 200 μm and 100 μm (enlarged graph). (D and E) Quantification of IHC results in (C). The percent of CCL-18 positive cells in primary and recurrent glioma samples accepting radiotherapy (D), and without radiotherapy (E). Data were presented as paired individual value (two-tailed paired t test, ∗ p < 0.05). (F) The correlation between tumor volume doubling time and the level of CCL-18. Data were presented as Pearson correlation coefficient. (G) Kaplan-Meier curves showing the progression free survival probability of glioma patients accepting radiotherapy based on different expression levels of CCL-18. Data were presented as median ± 95% confidence intervals (∗∗ p < 0.01). Data were obtained from 15 paired primary glioma and recurrent glioma with radiotherapy, and 8 paired primary glioma and recurrent glioma without radiotherapy (C–G).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Analysis, Immunohistochemistry, Irradiation, Two Tailed Test, Expressing

Multivariate Cox regression analysis from TCGA

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Multivariate Cox regression analysis from TCGA

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Analysis, Expressing

Radiation promotes macrophage to polarize into M2-TAMs, accompanying CCL-18 secretion (A) The mRNA level of CD163 and IL-10 after treatment with PMA or PMA+IL-4/13 on THP-1 cells. Data were presented as mean ± SEM (unpaired t test, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative immunoblot of CD163 and CD68 after PMA or PMA+IL-4/13 treatment in THP-1 cells. (C) Representative immunoblot of CD163 and CD68 after PMA treatment with or without different radiation doses. (D) The mRNA level of CD163 and IL-10 following the indicated treatment at different durations. Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.22, p = 0.32, ∗∗∗ p < 0.001; in IL-10: F = 1.82, p = 0.14, ∗∗∗ p < 0.001). (E) Representative immunoblot of CD163 and CD68 following the indicated treatment. (F) Representative immunofluorescence images of CD163 and CD68 staining following the indicated treatment. Scale bars: 200 μm. (G and H) Quantitative results of relative mean density of CD163 (G) and CD68 (H). Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.36, p = 0.3, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in CD68: F = 1.54, p = 0.26, ∗ p < 0.05, ∗∗ p < 0.01). (I) Representative immunoblot of indicated antibodies on THP-1 cells after PMA treatment with or without radiation. (J and K) The mRNA level (J) and the protein abundance (K) of CCL-18 following the indicated treatment. Data were presented as mean ± SEM (one-way ANOVA, in mRNA: F = 1.35, p = 0.27, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in protein: F = 3, p = 0.04, ∗∗∗ p < 0.001). Data were obtained from 4 independent experiments (A, F–H, and K), 3 independent experiments (B, C, E, and I) and 6 independent experiments (D and J).

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: Radiation promotes macrophage to polarize into M2-TAMs, accompanying CCL-18 secretion (A) The mRNA level of CD163 and IL-10 after treatment with PMA or PMA+IL-4/13 on THP-1 cells. Data were presented as mean ± SEM (unpaired t test, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative immunoblot of CD163 and CD68 after PMA or PMA+IL-4/13 treatment in THP-1 cells. (C) Representative immunoblot of CD163 and CD68 after PMA treatment with or without different radiation doses. (D) The mRNA level of CD163 and IL-10 following the indicated treatment at different durations. Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.22, p = 0.32, ∗∗∗ p < 0.001; in IL-10: F = 1.82, p = 0.14, ∗∗∗ p < 0.001). (E) Representative immunoblot of CD163 and CD68 following the indicated treatment. (F) Representative immunofluorescence images of CD163 and CD68 staining following the indicated treatment. Scale bars: 200 μm. (G and H) Quantitative results of relative mean density of CD163 (G) and CD68 (H). Data were presented as mean ± SEM (one-way ANOVA, in CD163: F = 1.36, p = 0.3, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in CD68: F = 1.54, p = 0.26, ∗ p < 0.05, ∗∗ p < 0.01). (I) Representative immunoblot of indicated antibodies on THP-1 cells after PMA treatment with or without radiation. (J and K) The mRNA level (J) and the protein abundance (K) of CCL-18 following the indicated treatment. Data were presented as mean ± SEM (one-way ANOVA, in mRNA: F = 1.35, p = 0.27, ∗∗ p < 0.01, ∗∗∗ p < 0.001; in protein: F = 3, p = 0.04, ∗∗∗ p < 0.001). Data were obtained from 4 independent experiments (A, F–H, and K), 3 independent experiments (B, C, E, and I) and 6 independent experiments (D and J).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Western Blot, Immunofluorescence, Staining, Quantitative Proteomics

CCL-18 does not mediate glioma cell proliferation following radiotherapy in vitro (A) Viability of GBM cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 1.9, p = 0.21, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative images of colony formation assay after CCL-18 (100 ng/mL) treatment. (C) Quantitative results from (B). Data were presented as mean ± SD (unpaired t test, ∗∗∗ p < 0.001). (D) Schematic workflow for the co-culture experiment. (E) Representative images of colony formation assay. (F) Quantitative results from (E). Data were presented as mean ± SD (unpaired t test, ∗ p < 0.05). (G) The mRNA level of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. Data were presented as mean ± SEM (unpaired t test, ∗∗∗ p < 0.001). (H) Representative immunoblot of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. (I) Quantitative results from (H). Data were presented as mean ± SEM (unpaired t test, ∗ p < 0.05, ∗∗ p < 0.01). (J) Immunoblot of CCR8 after overexpression. (K) Representative images of colony formation assay on irradiated GBM cells after CCL-18 (100 ng/mL) treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (two-way ANOVA, F = 4.9, p = 0.06, ∗ p < 0.05, ∗∗ p < 0.01). Data were obtained from 3 independent experiments (A–L).

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 does not mediate glioma cell proliferation following radiotherapy in vitro (A) Viability of GBM cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 1.9, p = 0.21, ∗∗ p < 0.01, ∗∗∗ p < 0.001). (B) Representative images of colony formation assay after CCL-18 (100 ng/mL) treatment. (C) Quantitative results from (B). Data were presented as mean ± SD (unpaired t test, ∗∗∗ p < 0.001). (D) Schematic workflow for the co-culture experiment. (E) Representative images of colony formation assay. (F) Quantitative results from (E). Data were presented as mean ± SD (unpaired t test, ∗ p < 0.05). (G) The mRNA level of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. Data were presented as mean ± SEM (unpaired t test, ∗∗∗ p < 0.001). (H) Representative immunoblot of PITPNM3, GPR30, and CCR8 on irradiated GBM cells. (I) Quantitative results from (H). Data were presented as mean ± SEM (unpaired t test, ∗ p < 0.05, ∗∗ p < 0.01). (J) Immunoblot of CCR8 after overexpression. (K) Representative images of colony formation assay on irradiated GBM cells after CCL-18 (100 ng/mL) treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (two-way ANOVA, F = 4.9, p = 0.06, ∗ p < 0.05, ∗∗ p < 0.01). Data were obtained from 3 independent experiments (A–L).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: In Vitro, Colony Assay, Co-culture Assay, Irradiation, Western Blot, Over Expression

CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet: CCL-18 do not mediate glioma recurrence following radiotherapy in vivo (A) Viability of GL261 cells after treatment with different concentrations of CCL-18. Data were presented as mean ± SEM (one-way ANOVA, F = 0.9, p = 0.48, ∗∗∗ p < 0.001). (B) Viability of GL261 cells after treatment with CCL-18 (100 ng/mL) and R243 (50, 100 μM). Data were presented as mean ± SEM (one-way ANOVA, F = 1.43, p = 0.28, ∗ p < 0.05, ∗∗∗ p < 0.001). (C) Representative immunoblot of ACP5, Akt, and phosphorylated Akt on GL261 cells after CCL-18 (100 ng/mL) treatment. (D) Schematic workflow for the cell-derived allograft experiment. (E) The bioluminescence value in mice receiving radiation on the indicated days. Data were presented as mean ± SEM (one-way ANOVA, in radiation: F = 2.48, p = 0.1, ∗ p < 0.05; in radiation with CCL-18 treatment: F = 1.41, p = 0.3, ∗ p < 0.05). (F) Representative pseudo-color bioluminescence images of intracranial allografts receiving radiation with or without CCL-18 administration. (G) Quantitative results from (F) on the indicated days. Data were presented as mean ± SEM (two-way ANOVA, F = 2.39, p = 0.04, ∗ p < 0.05, ∗∗ p < 0.01). (H) Kaplan-Meier curve showing the percent survival of mice receiving different treatment. Data were presented as median (∗∗∗ p < 0.001). (I) The percent of M1-TAM in glioma after radiation with or without CCL-18 treatment. (J) Quantitative results from (I). Data were presented as mean ± SD (one-way ANOVA, F = 1.46, p = 0.26). (K)The percent of M2-TAM in glioma after radiation with or without CCL-18 treatment. (L) Quantitative results from (K). Data were presented as mean ± SD (one-way ANOVA, F = 0.1, p = 0.9). Data were obtained from 3 independent experiments (A, C, and I–L), and 4 independent experiments (B). Data were obtained from ≥6 mice (E), ≥11 mice (G and H), and 3 mice (I–L).

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: In Vivo, Western Blot, Derivative Assay

Journal: iScience

Article Title: M2 type tumor-associated macrophage-derived CCL-18 promotes glioma cell proliferation but does not mediates glioma recurrence after radiotherapy

doi: 10.1016/j.isci.2026.117695

Figure Lengend Snippet:

Article Snippet: recombinant CCL-18 , Med Chem Express , HY-P7265.

Techniques: Cell-Signaling, Virus, Tissue, Microarray, Recombinant, cDNA Synthesis, Enzyme-linked Immunosorbent Assay, Software, Biomarker Discovery, In Vivo Imaging

Human CCL15 promotes the activation, proliferation, and migration of human intestinal fibroblasts. (A) Representative images of Masson's trichrome staining and IHC showing fibrosis levels and hCCL15 expression in stenotic and non‐stenotic intestinal surgical specimens from patients with CD. Scale bar: 500 µm (low magnification) and 100 µm (high magnification). n = 4 patients; 3 fields per zone. (B) Relative CCL15 mRNA abundance in stricture versus non‐stricture regions was quantified by RT‐qPCR. (C) Serum concentrations of hCCL15 in CD patients with or without intestinal strictures were detected using ELISA. (D) Correlation analysis between CCL15 and collagen‐associated genes ( COL1A1, COL6A1, COL3A1 , and FN1 ) in CD intestines. (E) Human intestinal fibroblasts (HIFs) isolated from stenotic regions were treated with recombinant CCL15 (5,10, and 20 ng/mL) for 48 h, and COL1A1 protein levels were then assessed by Western blot. (F–H) HIFs were stimulated with hCCL15 (10 ng/mL) for 48 h. Migration was assessed by wound healing assay (F; Scale bar: 500 µm). α‐SMA and Ki67 immunofluorescence staining was performed to evaluate activation and proliferation, and Ki67+ cells were quantified (G; Scale bar: 100 µm). mRNA levels of ACTA2 , COL1A1 , COL3A1 , COL6A1 , COL6A3 , and FN1 were measured by RT‐qPCR (H). I) Immunofluorescence co‐localization analysis of S100A8/A9 + CCL15 + macrophages and CCR1 + α‐SMA + fibroblasts in intestinal stricture sections from patients with CD. Red arrows indicate S100A8/A9 + CCL15 + macrophages located within 30 µm of the nearest fibroblast; white arrows indicate CCR1 + fibroblasts. Scale bars: 50 µm (low magnification) and 20 µm (high magnification). n = 4 patients; 3 fields per zone. All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.

Journal: Advanced Science

Article Title: S100A8/A9‐High Macrophages Activate Intestinal Fibroblasts via mCCL6/hCCL15‐CCR1 Axis to Drive Intestinal Fibrosis in Crohn's Disease

doi: 10.1002/advs.76353

Figure Lengend Snippet: Human CCL15 promotes the activation, proliferation, and migration of human intestinal fibroblasts. (A) Representative images of Masson's trichrome staining and IHC showing fibrosis levels and hCCL15 expression in stenotic and non‐stenotic intestinal surgical specimens from patients with CD. Scale bar: 500 µm (low magnification) and 100 µm (high magnification). n = 4 patients; 3 fields per zone. (B) Relative CCL15 mRNA abundance in stricture versus non‐stricture regions was quantified by RT‐qPCR. (C) Serum concentrations of hCCL15 in CD patients with or without intestinal strictures were detected using ELISA. (D) Correlation analysis between CCL15 and collagen‐associated genes ( COL1A1, COL6A1, COL3A1 , and FN1 ) in CD intestines. (E) Human intestinal fibroblasts (HIFs) isolated from stenotic regions were treated with recombinant CCL15 (5,10, and 20 ng/mL) for 48 h, and COL1A1 protein levels were then assessed by Western blot. (F–H) HIFs were stimulated with hCCL15 (10 ng/mL) for 48 h. Migration was assessed by wound healing assay (F; Scale bar: 500 µm). α‐SMA and Ki67 immunofluorescence staining was performed to evaluate activation and proliferation, and Ki67+ cells were quantified (G; Scale bar: 100 µm). mRNA levels of ACTA2 , COL1A1 , COL3A1 , COL6A1 , COL6A3 , and FN1 were measured by RT‐qPCR (H). I) Immunofluorescence co‐localization analysis of S100A8/A9 + CCL15 + macrophages and CCR1 + α‐SMA + fibroblasts in intestinal stricture sections from patients with CD. Red arrows indicate S100A8/A9 + CCL15 + macrophages located within 30 µm of the nearest fibroblast; white arrows indicate CCR1 + fibroblasts. Scale bars: 50 µm (low magnification) and 20 µm (high magnification). n = 4 patients; 3 fields per zone. All values are expressed as mean ± SD. ns, no significant difference, * p < 0.05, ** p < 0.01, *** p < 0.001.

Article Snippet: For treatment, HIFs were exposed to recombinant CCL15 (HY‐P7266, MCE, USA) at concentrations of 5, 10, or 20 ng/mL for 48 h; the 10 ng/mL dose was optimized for subsequent assays.

Techniques: Activation Assay, Migration, Staining, Expressing, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay, Isolation, Recombinant, Western Blot, Wound Healing Assay, Immunofluorescence