primary antibodies targeting cd68  (Novus Biologicals)

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: Primary antibodies targeting CD68 (1:500, Proteintech, 28058-1-AP), CXCL7 (1:500, Affinity, #DF6695), and CK (1:500, Affinity, #DF3072) were applied and incubated at room temperature for one hour.

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: Primary antibodies targeting CD68 (1:500, Proteintech, 28058-1-AP), CXCL7 (1:500, Affinity, #DF6695), and CK (1:500, Affinity, #DF3072) were applied and incubated at room temperature for one hour.

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

Journal: Kidney international

Article Title: Kidney injury-mediated disruption of intestinal lymphatics involves dicarbonyl-modified lipoproteins.

doi: 10.1016/j.kint.2021.05.028

Figure Lengend Snippet: Figure 6 | Proteinuric kidney injury stimulates ileal macrophage production of vascular endothelial growth factor (VEGF)-C. (a) Puromycin aminoglycoside (PAN) increased ileal VEGF-C versus controls (Cont). (b) VEGF-C concentration in PAN lymph was lower, but total output of VEGF-C was significantly greater, in PAN versus Cont. (c) Double staining of ileum with VEGF-C (red) and cluster of differentiation (CD) 68 (green) showed a greater number of CD68-positive cells and CD68- and VEGF-C–positive cells (arrows) in PAN versus Cont. (d) Cultured macrophages exposed to isolevuglandin (IsoLG)–apolipoprotein AI (apoAI) expressed more VEGFC mRNA versus unmodified apoAI. In vivo, results are mean SD for 7 to 12 rats per group. In vitro, experiments were performed independently 3 times with 3 wells per treatment. To optimize viewing of this image, please see the online version of this article at www.kidney-international.org.

Article Snippet: Double staining for CD68 and VEGF-C used citrate buffer for antigen retrieval, followed by biotinylated primary antibody targeting CD68 (1:10; BioRad).

Techniques: Concentration Assay, Double Staining, Cell Culture, In Vivo, In Vitro