human cxcl7 nap 2 duoset elisa kit  (R&D Systems)

Journal: Journal of Neuroinflammation

Article Title: CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain

doi: 10.1186/s12974-025-03679-x

Figure Lengend Snippet: Increased inflammatory and oxidative stress levels in the PVT of DIO mice. A Quantification of CXCL7 in plasma from control or DIO mice. n = 3 mice per group, P = 0.0003. B and C Representative images ( B ) and summarized data ( C ) of the expression of CXCL7 in PVT Glu neurons from control and DIO mice. n = 5 mice per group, with one slice from each mouse. P < 0.0001. Scale bars, 10 μm. D - H Representative images ( D ) and quantification of IBA1 + cell numbers ( E ), intensity ( F ) and Imaris-based semiautomatic quantification of cell morphometry, including total branch length ( G ) and points ( H ) of IBA1 + -microglia from control and DIO mice. n = 5 mice per group for quantification of cell number and intensity, with one slice from each mouse. P (number) = 0.0081, P (intensity) = 0.0122. n= 6 mice for the control group and n = 7 mice for the DIO group in the quantification of branch length and points, with one slice from each mouse. P (length) = 0.014, P (intensity) = 0.0001. Scale bars, 10 μm (overview) and 3 μm (inset and rendering). I and J Representative images ( I ) and summarized data ( J ) of GPX4 in PVT Glu neurons from control and DIO mice. n = 6 mice per group, with one slice from each mouse. P = 0.0012. Scale bars, 10 μm. Statistical analysis was performed using Student’s t test. * P < 0.05, ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Seven days later, a volume of 50 ng/μl CXCL7 protein (HY- P75698 , MCE, USA) dissolved in artificial cerebrospinal fluid (ACSF) was infused into the lateral ventricles (1 μl), or PVT (300 nl) was given once a day for three days in a row.

Techniques: Clinical Proteomics, Control, Expressing

Journal: Journal of Neuroinflammation

Article Title: CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain

doi: 10.1186/s12974-025-03679-x

Figure Lengend Snippet: Infusion of CXCL7 improved PVT Glu neuronal activity and induced pain hypersensitivity in control mice. A Schematic of the experimental procedure. B Image showing the site of the cannula implanted in the lateral ventricle of control mice. Scale bar, 500 μm. C and D Effects of infusion of CXCL7 in the lateral ventricle on the pain threshold in control mice treated with ACSF or CXCL7, using von Frey test ( C ) and Hargreaves tests ( D ). n = 5 mice per group, P = 0.0079 ( C ), P = 0.0007 ( D ). E Representative heatmaps of travel trajectory of control mice treated with ACSF or CXCL7 in the CPA test. F and G Summarized data of aversion index ( F ) and preference index ( G ) for ( E ), n = 7 mice per group. P < 0.0001 ( F and G ). ( H ) Image showing the site of the cannula implanted in the PVT of control mice. Scale bar, 500 μm. I and J Representative images ( I ) and summarized data ( J ) of CXCL7 on PVT Glu neurons in control mice treated with ACSF or CXCL7. n = 6 mice, with one slice from each mouse, P < 0.0001. Scale bar, 10 μm. K and L Representative images ( K ) and summarized data ( L ) of c-Fos in PVT from control mice treated with ACSF or CXCL7. n = 5 mice, with one slice from each mouse. P = 0.0061. Scale bar, 200 μm. M and N Sample traces ( M ) and summarized number of spikes ( N ) in PVT Glu neurons recorded from control mice treated with ACSF or CXCL7. n = 14 cells from 4 mice per group. P (time × column factor) = 0.0019, P (time) < 0.0001, P (column factor) = 0.001, F (1, 26) = 13.79. O and P Effects of the infusion of CXCL7 in PVT Glu neurons on the pain threshold using the von Frey test ( O ) and Hargreaves tests ( P ) of control mice treated with ACSF or CXCL7. n = 7 mice per group, P = 0.0002 ( O ), P = 0.0015 ( P ). Q Representative heatmaps of travel trajectory of control mice treated with ACSF or CXCL7 within PVT in the CPA test. ( R and S ) Summarized data of aversion index ( R ) and preference index ( S ) for ( Q ), n = 7 mice per group. P = 0.0003 ( R and S ). Statistical analysis was performed using Student’s t test in ( C ), ( D) , ( F) , ( G) , ( J) , ( L) , ( O) , ( P) , ( R) and ( S ), and two-way ANOVA followed by Bonferroni’s post hoc correction in ( N ). ** P < 0.01, *** P < 0.001, **** P < 0.0001

Article Snippet: Seven days later, a volume of 50 ng/μl CXCL7 protein (HY- P75698 , MCE, USA) dissolved in artificial cerebrospinal fluid (ACSF) was infused into the lateral ventricles (1 μl), or PVT (300 nl) was given once a day for three days in a row.

Techniques: Activity Assay, Control

Journal: Journal of Neuroinflammation

Article Title: CXCL7/CXCR2 in the paraventricular thalamus mediates obesity-related pain

doi: 10.1186/s12974-025-03679-x

Figure Lengend Snippet: Mechanism of CXCL7-CXCR2 interaction in PVT Glu →BLA Glu neuronal circuit promotes the onset of obesity-related pain. In obese mice, elevated expression of the chemokine, CXCL7, results in the binding of CXCR2 receptors of PVT Glu neurons, thereby leading to increased activity in PVT Glu →BLA Glu neuronal circuit, which mediate obesity-related pain

Article Snippet: Seven days later, a volume of 50 ng/μl CXCL7 protein (HY- P75698 , MCE, USA) dissolved in artificial cerebrospinal fluid (ACSF) was infused into the lateral ventricles (1 μl), or PVT (300 nl) was given once a day for three days in a row.

Techniques: Expressing, Binding Assay, Activity Assay

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 1 CXCL7 upregulation in chemotherapy-resistant colorectal cancer. A Differential gene expression profiling between chemosensitive and chemoresistant colorectal tumors (TCGA cohort) treated with 5-FU/oxaliplatin combination therapy. B Representative immunohisto- chemical (IHC) staining of CXCL7 in chemotherapy-resistant versus chemotherapy-sensitive CRC specimens (Scale bar, 100 μm). C Gene Set Enrichment Analysis (GSEA) demonstrating cisplatin resistance pathway activation in CXCL7-high versus CXCL7-low expression subgroups. D Comparative histopathological analysis using H&E staining and IHC evaluation of CXCL7/CD68 expression in paired pre- and post- chemotherapy CRC specimens from individual patients (Scale bar, 100 μm). E CXCL7 protein localization by IHC in chemotherapy-treated CRC lesions versus matched adjacent normal mucosa (Scale bar, 100 μm). F Quantitative comparison of CXCL7 expression levels between chemotherapeutically treated malignant tissues and non-neoplastic colorectal tissues. G Stage-dependent IHC expression patterns of CXCL7 across colorectal cancer progression (Scale bar, 100 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not significant.

Article Snippet: CT26 murine colorectal cancer cells were subcutaneously injected into BALB/c mice, followed by treatment with anti-CXCL7 antibody (20 μg/mouse, R&D Systems, AF793) or isotype control antibodies, with tumor volume monitoring and subsequent tumor collection for apoptosis assays and IHC analysis.

Techniques: Gene Expression, Immunohistochemistry, Activation Assay, Expressing, Staining, Comparison

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 2 Macrophage-derived CXCL7 promotes chemoresistance in colorectal cancer cells. A CXCL7-associated single-cell analysis of CRC_GSE146771 using the TISCH2 database. B Correlation analysis of CXCL7 with macrophage infiltration via TCGA database. C Left: mIHC staining of chemotherapy-sensitive versus resistant CRC tissues showing CK+ (purple), CXCL7+ (white), and CD68+ macrophages (green), with DAPI nuclear staining (blue) (scale bar, 50 μm). Right: CXCL7+ macrophage proportions in chemotherapy-sensitive versus resistant patients. D Schematic of tumor cell-macrophage co-culture system. E CXCL7 mRNA and F CXCL7 protein levels in macrophages co-cultured with HCT116 cells ± 5-FU (5 μM), oxaliplatin (5 μM), or combination. F The expression of CXCL7 in chemotherapy-treated colorectal cancer tissues compared with non-tumor tissues was analyzed. G Representative images and quantification for colony formation of CRC cells with CXCL7 + Mø versus CXCL7- Mø under 5-FU/oxaliplatin treatment. H Annexin V/PI apoptosis rates and (I) TUNEL+ cells (green) in CRC cells co-cultured with CXCL7 + Mø versus CXCL7- Mø under chemotherapy (scale bar, 50 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not significant.

Article Snippet: CT26 murine colorectal cancer cells were subcutaneously injected into BALB/c mice, followed by treatment with anti-CXCL7 antibody (20 μg/mouse, R&D Systems, AF793) or isotype control antibodies, with tumor volume monitoring and subsequent tumor collection for apoptosis assays and IHC analysis.

Techniques: Derivative Assay, Single-cell Analysis, Staining, Co-Culture Assay, Cell Culture, Expressing, TUNEL Assay

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 3 CXCL7 Mediates Tumor Chemotherapy Resistance in vivo. A Representative images and body weights of mice injected with CXCL7 + Mø or CXCL7- Mø under 5-FU/oxaliplatin treatment (n = 5 mice per group). B CT26 tumor growth in immunocompetent BALB/c mice treated with control or macrophage depletion (n = 5 mice per group). C CXCL7 expression levels in macrophage-intact versus macrophage- depleted tumors analyzed by RT-qPCR. D IHC staining of CD11b+ cells and CXCL7+ expression in control versus clodronate-treated tumors (scale bar, 50 μm). E CT26 tumor progression in mice treated with isotype control or CXCL7-neutralizing antibodies (n = 5 mice per group). F TUNEL-positive cells and representative IHC images of CXCL7 in the tumors obtained from mice treated with isotype control or CXCL7 neutralizing antibodies (scale bar for TUNEL, 10 μm; scale bar for IHC, 100 μm). G Intestinal polyp quantification (number/size) and representative images from AOM/DSS mice treated with control or CXCL7-neutralizing antibodies (scale bar, 100 μm). H HE and IHC detection of CXCL7 expression across different groups of mice, as indicated (scale bar, 100 μm). I TUNEL+ apoptotic cell counts in AOM/DSS mice with/ without CXCL7 antibody treatment. All data are presented as mean ± SD. *P < 0.05; n.s.not significant.

Article Snippet: CT26 murine colorectal cancer cells were subcutaneously injected into BALB/c mice, followed by treatment with anti-CXCL7 antibody (20 μg/mouse, R&D Systems, AF793) or isotype control antibodies, with tumor volume monitoring and subsequent tumor collection for apoptosis assays and IHC analysis.

Techniques: In Vivo, Injection, Control, Expressing, Quantitative RT-PCR, Immunohistochemistry, TUNEL Assay

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 4 CXCL7 upregulates PHGDH and activates serine metabolism in cancer cells. A Left: GSEA of enriched pathways in differentially expressed genes (DEGs) between HT29-control and HT29-CXCL7 groups. Right: Comparative analysis of PHGDH FPKM values between groups. B The expression level of PHGDH in control and CXCL7-overexpressing cells with or without the CXCR2 inhibitor, as determined by RT-qPCR. C Western blot detection of serine biosynthesis enzymes (PHGDH, PSAT1, PSPH).GAPDH was used as the loading control. D Kaplan‒Meier analysis of overall survival in TCGA-CRC patients stratified by PHGDH expression. E Left: Metabolite enrichment pathway bubble plot. Middle: Heatmap of differential metabolites. Right: Schematic of serine/one-carbon metabolism. F Heatmap visualization of DEGs in glycine, serine, and threonine metabolism pathways. G ELISA analysis of SAM levels in CXCL7-overexpressing cells and PHGDH-inhibited cells. H TUNEL assays of CXCL7-overexpressing cells transfected with NC-siRNA or PHGDH-siRNA, with or without SAM treatment(scale bar, 50 μm). I The drug sensitivity of CXCL7-overexpressing cells transfected with NC-siRNA or PHGDH-siRNA, with or without SAM treatment. All data are presented as mean ± SD. *P < 0.05; n.s.not significant.

Article Snippet: CT26 murine colorectal cancer cells were subcutaneously injected into BALB/c mice, followed by treatment with anti-CXCL7 antibody (20 μg/mouse, R&D Systems, AF793) or isotype control antibodies, with tumor volume monitoring and subsequent tumor collection for apoptosis assays and IHC analysis.

Techniques: Control, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, TUNEL Assay, Transfection

Journal: Cell death & disease

Article Title: Chemotherapy-induced macrophage CXCL7 expression drives tumor chemoresistance via the STAT1/PHGDH-serine metabolism axis and SAM paracrine feedback to M2 polarization.

doi: 10.1038/s41419-025-07712-y

Figure Lengend Snippet: Fig. 5 STAT1 mediates CXCL7-induced PHGDH transcription and chemotherapy resistance. A GSEA analysis illustrating the correlation between CXCL7 and the interferon signaling pathway. B Predicted STAT1-binding sequences in the PHGDH promoter region using the JASPAR database. C The correlationship between STAT1 and PHGDH mRNA expression. D ChIP-qPCR results showing STAT1 enrichment at the PHGDH promoter. E Luciferase reporter assay results demonstrating PHGDH promoter activity in response to CXCL7 treatment with or without JAK1 inhibition. F Effects of JAK1 inhibition on PHGDH mRNA expression following CXCL7 treatment. G Western blot analysis of p-JAK1, JAK1, p-STAT1, STAT1, PHGDH, and IRF9 protein levels in cells treated with CXCL7 with or without JAK1 inhibition. H Cell viability assessment for cell treatment with CXCL7, following PHGDH inhibition or JAK1 inhibition. I Effects of PHGDH or JAK1 inhibition on tumor growth in mice with CXCL7-overexpressing cell. J IHC analysis of p-STAT1, PHGDH, and CD206 expression, along with TUNEL staining for apoptosis, in CXCL7-overexpressing tumors treated with PHGDH or JAK1 inhibitor (scale bar for IHC, 50 μm; scale bar for TUNEL, 10 μm). All data are presented as mean ± SD. *P < 0.05; n.s.not significant.

Article Snippet: CT26 murine colorectal cancer cells were subcutaneously injected into BALB/c mice, followed by treatment with anti-CXCL7 antibody (20 μg/mouse, R&D Systems, AF793) or isotype control antibodies, with tumor volume monitoring and subsequent tumor collection for apoptosis assays and IHC analysis.

Techniques: Binding Assay, Expressing, ChIP-qPCR, Luciferase, Reporter Assay, Activity Assay, Inhibition, Western Blot, Paraffin-embedded Immunohistochemistry, TUNEL Assay, Staining