Journal: Proteome science

Article Title: Identification of noval diagnostic biomarker for HFpEF based on proteomics and machine learning.

doi: 10.1186/s12953-025-00242-7

Figure Lengend Snippet: Fig. 6 Expression analysis of hub proteins in immune cells. (A) Expression of ITIH 4 in immune cells. (B) Expression of SERPINA1 in immune cells

Article Snippet: Plasma SERPINA3 levels were measured by ELISA kit SERPINA3(Human SERPINA3 ELISA Kit YX-E11217, sinobestbio), ITIH4 (Human ITIH4 ELISA Kit EK1670 BOSTER), SERPINA1 (Human Alpha 1 Antitrypsin/SERPINA1 ELISA Kit EK1634 BOSTER), AFM (Human Afamin/AFM ELISA Kit (EK1487 BOSTER) according to the manufacturer’s instructions.

Techniques: Expressing

Journal: Proteome science

Article Title: Identification of noval diagnostic biomarker for HFpEF based on proteomics and machine learning.

doi: 10.1186/s12953-025-00242-7

Figure Lengend Snippet: Fig. 7 Expression of feature proteins in tissue-specific analysis. (A) Expression of SERPINA3 in tissue-specific analysis. (B) Expression of SERPINA1 in tissue- specific analysis. (C) Expression of AFM in tissue-specific analysis. (D) Expression of ITIH4 in tissue-specific analysis

Article Snippet: Plasma SERPINA3 levels were measured by ELISA kit SERPINA3(Human SERPINA3 ELISA Kit YX-E11217, sinobestbio), ITIH4 (Human ITIH4 ELISA Kit EK1670 BOSTER), SERPINA1 (Human Alpha 1 Antitrypsin/SERPINA1 ELISA Kit EK1634 BOSTER), AFM (Human Afamin/AFM ELISA Kit (EK1487 BOSTER) according to the manufacturer’s instructions.

Techniques: Expressing

Journal: Proteome science

Article Title: Identification of noval diagnostic biomarker for HFpEF based on proteomics and machine learning.

doi: 10.1186/s12953-025-00242-7

Figure Lengend Snippet: Fig. 8 The expression profile analysis of feature proteins. (A) SERPINA3 expression in clinical plasma samples. (B) SERPINA1 expression in clinical plasma samples. (C) AFM expression in clinical plasma samples. (D) ITIH4 expression in clinical plasma samples

Article Snippet: Plasma SERPINA3 levels were measured by ELISA kit SERPINA3(Human SERPINA3 ELISA Kit YX-E11217, sinobestbio), ITIH4 (Human ITIH4 ELISA Kit EK1670 BOSTER), SERPINA1 (Human Alpha 1 Antitrypsin/SERPINA1 ELISA Kit EK1634 BOSTER), AFM (Human Afamin/AFM ELISA Kit (EK1487 BOSTER) according to the manufacturer’s instructions.

Techniques: Expressing, Clinical Proteomics

Journal: Journal for Immunotherapy of Cancer

Article Title: Cell membrane-anchored and tumor-targeted IL-12 T-cell therapy destroys cancer-associated fibroblasts and disrupts extracellular matrix in heterogenous osteosarcoma xenograft models

doi: 10.1136/jitc-2023-006991

Figure Lengend Snippet: Membrane-anchored and tumor-targeted IL-12 (attIL12)-T cell treatment upregulates FAS expression on the cell surface of cancer-associated fibroblasts (CAFs). (A–C) CAFs were cocultured with the indicated T cells (1:3 ratio) in OSD-conditioned medium (OSD CM) with or without the cell-surface vimentin (CSV)-blocking antibody 84–1 (10 µg/mL) for 48 hours (n=3). (A) FAS expression on OS1 and OS2 CAFs as determined by flow cytometry. Graphs show the percentages (mean±SEM) of FAS + CAFs. (B) Violin plot showing the concentrations (mean±SEM) of interferon gamma (IFNγ) in supernatant as determined by ELISA. (C) Violin plot shows the transforming growth factor beta (TGFβ) level (mean±SEM) in supernatant as determined via ELISA. (D, E, F) CAFs were cocultured with T cells (1:3 ratio) in OSD CM with or without an IFNγ-blocking antibody (10 µg/mL) (n=3). (D) FAS expression on OS1 and OS2 CAFs as determined by flow cytometry. Graphs show the percentages (mean±SEM) of FAS + CAFs. (E) Suspended T cells were removed from the coculture system after 48 hours. Immunoblots of FAS, cleaved caspase 3, total caspase 3, BcL-xL, cleaved PARP, α-SMA, and GAPDH in OS1 and OS2 CAFs are shown. (F) Caspase 3/7 expression on OS1 and OS2 CAFs as determined by flow cytometry. Graphs show the percentages (mean±SEM) of cas3/7 + CAFs. (G) Immunofluorescence staining and whole-slide staining of OS1 and OS33 tumor sections stained with fibroblast activation protein (FAP) (red), α-smooth muscle actin (αSMA) (yellow), Fas (green), and Hoechst (blue). Scale bar: 500 µm. **p<0.01; ***p<0.001; ****p<0.0001.

Article Snippet: The levels of IFNγ, TGFβ, collagen, and fibronectin were measured by using ELISA Ready-SET-Go! kits (eBioscience) or ELISA Kit Picokine (Boster Bio).

Techniques: Membrane, Expressing, Blocking Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Western Blot, Immunofluorescence, Staining, Activation Assay

Journal: Cell Reports Medicine

Article Title: A functional cardiac patch promotes cardiac repair by modulating the CCR2 − cardiac-resident macrophage niche and their cell crosstalk

doi: 10.1016/j.xcrm.2025.101932

Figure Lengend Snippet:

Article Snippet: Rat CXCL4/PF4 ELISA Kit , Boster Bio. , EK1651.

Techniques: Recombinant, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Staining, Labeling, H&E Stain, Lysis, Software

Journal: Mediators of Inflammation

Article Title: Monocytes Undergo Functional Reprogramming to Generate Immunosuppression through HIF-1 α Signaling Pathway in the Late Phase of Sepsis

doi: 10.1155/2020/4235909

Figure Lengend Snippet: Its cytokine production in the blood serum. (a) In the clinical study, the higher levels of TNF- α , IL-1 β , IL-6, IL-18, CCL3, and CCL5 except for IL-10 in the early phase of sepsis compared with the late phase of sepsis and the healthy participants, n = 30. ∗∗ P < 0.01 represented the significant difference; ## P < 0.01: compared with the healthy participants, the difference was of significance. (b) Ade-HIF-1 α injection increased the production of TNF- α , IL-1 β , IL-6, IL-18, CCL3, and CCL5 except for IL-10 in the late stage of the sepsis rat model. ∗∗ P < 0.01: compared with the normal control group, the difference was of significance; # P < 0.05: compared with the sepsis rat model group and the adenovirus control group; & P < 0.05: compared with the sepsis rat model group. Besides, data were presented as mean ± standard deviation, and data was repeated in triplicate.

Article Snippet: Then, the serum of the blood samples was dividedly analyzed with ELISA assay kits as per the manufacturer's protocol to quantify the concentration of IL-1 β (catalog:70-EK101B-96, homo; catalog:70-EK201B/3-96, mus; MultiSciences, China), IL-18 (catalog: 70-EK118-48, homo; catalog: 70-EK218-96, mus; MultiSciences, China), IL-6 (catalog: 70-EK106/2-96, homo; catalog: 70-EK206/3-96, mus; MultiSciences, China), IL-10 (catalog: 70-EK110/2-96, homo; catalog: 70-EK210/3-96, mus; MultiSciences, China), TNF- α (catalog: 70-EK182-96, homo; catalog: 70-EK282/3-96, mus; MultiSciences, China), CCL3 (catalog: 70-EK161-96, homo; catalog: 70-EK261/2-96, mus; MultiSciences, China), and CCL5 (catalog: 70-EK1129-96, homo; catalog: 70-EK2129/2-96, mus; MultiSciences, China) in triplicates.

Techniques: Injection, Standard Deviation

Journal: Journal of Molecular Cell Biology

Article Title: CSF2 upregulates CXCL3 expression in adipocytes to promote metastasis of breast cancer via the FAK signaling pathway

doi: 10.1093/jmcb/mjad025

Figure Lengend Snippet: CSF2 is highly expressed in adipocytes and tumor cells after co-culture. ( A and B ) The expression ( A ) and secretion ( B ) of CSF2 in preadipocytes co-cultured with MDA-MB-231 cells for 0, 12, 24, and 48 h were measured by q-PCR and ELISA, respectively. ( C and D ) The expression ( C ) and secretion ( D ) of CSF2 in adipocytes co-cultured with MDA-MB-231 cells for 0, 12, 24, and 48 h. ( E and F ) Adipocytes were co-cultured with different breast cancer cells or normal mammary epithelial cells (MCF10A), and the expression ( E ) and secretion ( F ) of CSF2 were measured. ( G and H ) The expression ( G ) and secretion ( H ) of CSF2 in MDA-MB-231 and BT549 cells co-cultured with adipocytes. The relevant MDA-MB-231 or BT549 cells cultured alone served as the control. ( I ) The mRNA expression levels of CSF2 in normal mammary and breast cancer tissues were measured by q-PCR. *** P < 0.001, ** P < 0.01, * P < 0.05, and NS ( P > 0.05); n = 3.

Article Snippet: CSF2, CXCL1, CXCL2, CXCL3, and CXCL8 in conditioned culture supernatant of adipocytes or tumor cells were measured using ELISA kits (#EK163, #EK196, #EK1264, #EK1265, #EK108, MultiSciences).

Techniques: Co-Culture Assay, Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay, Control

Journal: Journal of Molecular Cell Biology

Article Title: CSF2 upregulates CXCL3 expression in adipocytes to promote metastasis of breast cancer via the FAK signaling pathway

doi: 10.1093/jmcb/mjad025

Figure Lengend Snippet: CSF2 activates Stat3 to upregulate CXCL3 expression in adipocytes co-cultured with breast cancer cells. ( A ) The mRNA expression levels of CSF2Rα and CSF2Rβ in adipocytes co-cultured with MDA-MB-231 cells were measured by q-PCR. ( B and C ) Cytokine expression ( B ) and secretion ( C ) in adipocytes treated with rhCSF2 (20 ng/ml) were detected by q-PCR and ELISA, respectively. ( D ) The mRNA expression levels of IL-6, CSF2, and CXCLs in normal and paracancerous adipose tissues. ( E ) Adipocytes were stimulated with rhCSF2 for 12 h and then treated with stattic (10 μM). The mRNA expression levels of CXCLs, IL-6, and IL-1β in adipocytes were detected. ( F ) Adipocytes were treated with rhCSF2 and stattic for 15 min, and Stat3 phosphorylation was analyzed by western blotting. ( G and H ) Adipocytes were co-cultured with MDA-MB-231 cells in the presence or absence of CSF2-neutralizing antibody (2 μg/ml). The expression of CXCLs ( G ) and Stat3 phosphorylation ( H ) in adipocytes were analyzed by q-PCR and western blotting, respectively. ### P < 0.001, ## P < 0.01, and # P < 0.05 compared to the control group; *** P < 0.001, ** P < 0.01, and * P < 0.05 compared to experimental group; n = 3.

Article Snippet: CSF2, CXCL1, CXCL2, CXCL3, and CXCL8 in conditioned culture supernatant of adipocytes or tumor cells were measured using ELISA kits (#EK163, #EK196, #EK1264, #EK1265, #EK108, MultiSciences).

Techniques: Expressing, Cell Culture, Enzyme-linked Immunosorbent Assay, Phospho-proteomics, Western Blot, Control

Journal: Journal of Inflammation Research

Article Title: Tumor-Infiltrating PD-L1+ Neutrophils Induced by GM-CSF Suppress T Cell Function in Laryngeal Squamous Cell Carcinoma and Predict Unfavorable Prognosis

doi: 10.2147/JIR.S347777

Figure Lengend Snippet: LSCC tumor microenvironment remodels and regulates the phenotype and function of neutrophils. ( A ) TCCS or cultural medium from AMC-HN-8 cells upregulated the level of immunosuppressive molecule PD-L1 on neutrophils. ( B ) ELISA detected the concentration of GM-CSF, G-CSF and TGF-β1 in the plasma, TCCS and NTCCS of LSCC patients. ( C ) Representative images were shown for GM-CSF IHC staining (magnification, X 50) of tumor tissues and normal tissues from LSCC patients. Bars = 500μm. ( D ) Cytokine GM-CSF most significantly upregulated the level of immunosuppressive molecule PD-L1 on neutrophils. ( E-G ) Representative histograms and statistics analysis of the proliferative capacity of CD4+T cells and CD8+ T cells following the coculture of PANs from LSCC patients with PBMCs at different stimuli. ( H and I ) IFN-γ and TNF-α production of T cells following the coculture of PANs from LSCC patients with PBMCs at different stimuli. ns = p > 0.05, *p < 0.05, **p < 0.01, ***p < 0.001.

Article Snippet: Commercial ELISA kits GM-CSF (70-EK1632, MultiSciences, Hangzhou, China), G-CSF (70-EK1692, MultiSciences, Hangzhou, China) and TGF-β1 (70-EK1812, MultiSciences, Hangzhou, China) were performed to assess the cytokines concentrations in the plasma of healthy controls and LSCC patients, and tissue supernatant of TCCS and NTCCS according to the manufacturers’ instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Concentration Assay, Clinical Proteomics, Immunohistochemistry