cxcl10 ip 10 levels (Elabscience Biotechnology)
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cxcl10 ip 10 levels
Cxcl10 Ip 10 Levels, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/interferongamma/Mouse+IP-10%2FCXCL10+(Interferon+Gamma+Induced+Protein+10kDa)+ELISA+Kit/pmc13655249-272-0-10
Average 94 stars, based on 26 article reviews
Cxcl10 Ip 10 Levels, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 26 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/interferongamma/Mouse+IP-10%2FCXCL10+(Interferon+Gamma+Induced+Protein+10kDa)+ELISA+Kit/pmc13655249-272-0-10
Average 94 stars, based on 26 article reviews
cxcl10 ip 10 levels - by Bioz Stars,
2026-10
94/100 stars
Images
1) Product Images from "Aged ZnO Nanoparticles Promote Breast Cancer Lung Metastasis by Remodeling the Pulmonary Microenvironment Through the CXCL10/Wnt/β‐Catenin Axis"
Article Title: Aged ZnO Nanoparticles Promote Breast Cancer Lung Metastasis by Remodeling the Pulmonary Microenvironment Through the CXCL10/Wnt/β‐Catenin Axis
Journal: Advanced Science
doi: 10.1002/advs.78249
Figure Legend Snippet: CXCL10 is upregulated in both macrophages and fibroblasts responding to aged ZnO NPs exposure. (A) Heatmaps exhibited multiplex cytokine profiling of serum and BALF from IT (PBS/fresh NPs/aged NPs intratracheal instillation) and IT + IV (IT exposure followed by intravenous injection of 4T1 cells) models ( n = 3). (B–E) Concentrations of significantly dyregulated cytokines in serum and BALF from mice exposed to ZnO NPs (fresh or aged), with or without subsequent 4T1 cell injection ( n = 3). (F) Venn plot showed the overlapping cytokines in serum and BALF between IT and IT + IV models. (G) ELISA detection of CXCL10 concentrations in serum and BALF of IT and IT + IV groups ( n = 3). (H) qPCR analysis of CXCL10 mRNA in lung tissue, primary fibroblasts, and alveolar macrophages post‐IT, normalized to GAPDH ( n = 3). (I, J) UMAP visualization (I) and dot plot (J) displaying CXCL10 expression across annotated cell types. (K, L) UMAP visualization (K) and dot plot (L) displaying CXCL10 expression across myeloid cell types. (M) Representative images of invasion and migration assays of 4T1 cells stimulated with 50 or 100 ng/mL murine recombinant CXCL10 (rCXCL10) for 72 h ( n = 3). (N) Quantification of invasion and migration assays ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p < 0.05, ** p < 0.01 vs control group; # p < 0.05, ## p < 0.01 vs fresh NPs group.
Techniques Used: Multiplex Assay, Profiling, Injection, Enzyme-linked Immunosorbent Assay, Analysis, Tissue, Expressing, Migration, Recombinant, Control
Figure Legend Snippet: CXCL10 silencing abrogates aged ZnO NPs–induced accumulation of pro‐metastatic stromal populations. (A) Schematic of coculture model: NIH‐3T3 or Raw264.7 cells with CXCL10 knockdown were stimulated with PBS, fresh or aged NPs (7.5 µg/mL), co‐cultured with 4T1 cells for 72 h. (B) qPCR analysis confirming CXCL10 knockdown in Raw264.7 cells ( n = 3). (C‐E) CXCL10 knockdown in Raw264.7 macrophages attenuates ZnO NP‐enhanced M2 polarization, as shown by reduced Arg1, Mrc1 expression (C) and CD206 + cell frequency (D, E) ( n = 3). (F) qPCR analysis confirming CXCL10 knockdown in NIH‐3T3 cells ( n = 3). (G, H) Flow cytometric analysis (G) and quantification (H) of the percentage of CD140a‐positive cells among CXCL10‐knockdown NIH‐3T3 cells in the co‐culture system ( n = 3). (I) qPCR analysis of CAF‐related genes (FN1, FSP1, α‐SMA, CD140a) in CXCL10‐knockdown NIH‐3T3 cells from the co‐culture model ( n = 3). (J) Schematic illustration of primary MDSCs preparation: primary mouse bone marrow‐derived macrophages were differentiated into MDSCs by supplement of GM‐CSF (40 ng/mL) and IL‐6 (40 ng/mL). MDSCs with CXCL10 knockdown were stimulated with PBS, fresh ZnO NPs, or aged ZnO NPs (7.5 µg/mL), then co‐cultured with 4T1 cells for 72 h. Cells were collected for further experiments. (K) qPCR analysis of relative CXCL10 mRNA expression in MDSCs with CXCL10 knockdown ( n = 3). (L, M) Flow cytometric analysis (L) and quantification (M) of the proportion of granulocytic CD11b + Ly6G + Ly6C low PMN‐MDSCs in the co‐culture system after CXCL10 knockdown ( n = 3). All data were represented as the mean ± SD. P values were calculated by one‐way ANOVA followed by Tukey's test. * p <0.05; ** p <0.01.
Techniques Used: Knockdown, Cell Culture, Analysis, Expressing, Co-culture Assay, Derivative Assay
Figure Legend Snippet: Pharmacological blockade of CXCL10/CXCR3 abrogates ZnO NP–enhanced metastasis. (A) Timeline of intraperitoneal administration of the CXCL10 receptor antagonist AMG487, ZnO NPs intratracheal instillation, and injection of 4T1‐Luc cells. (B–I) AMG487 treatment significantly reduced ZnO NP–induced lung metastatic burden, as shown by longitudinal and ex vivo bioluminescence (B–E), with corresponding decreases in lesion area (F, G) and tumor cell proliferation (Ki‐67) (H, I). Aged NP effects are more pronounced but similarly reversed by AMG487. ( n = 4). Scale bar (F): 2 mm (top) and 500 µm (bottom). Scale bar (H): 20 µm. (J) CXCL10/CXCR3 inhibition improves overall survival in ZnO NP‐exposed mice ( n = 10). (K) Schematic diagram of pulmonary niche remodeling by ZnO NPs exposure facilitating breast cancer metastasis via CXCL10/Wnt/beta‐catenin axis. All data were represented as the mean ± SD. P values were calculated by Kaplan‐Meier analysis in J, others with one‐way ANOVA followed by Tukey's test. * p <0.05; ** p <0.01.
Techniques Used: Injection, Ex Vivo, Inhibition, Analysis
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