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R&D Systems elisa kit
Elisa Kit, supplied by R&D Systems, used in various techniques. Bioz Stars score: 96/100, based on 366 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/quantikine+human+mcp+1+kit/Human+CCL2%2FMCP-1+Quantikine+ELISA+Kit/pm42024456-240-11-14
Average 96 stars, based on 366 article reviews

elisa kit - by Bioz Stars, 2026-09

96/100 stars

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Enzyme-linked Immunosorbent Assay:

Article Title: Methods and compositions for the treatment of inflammatory diseases
Article Snippet: .. MCP-1 ELISA was carried out using Quantikine Human MCP-1 kit as described by manufacturer (R&D Systems). ..

Article Title: Lipoic Acid Synthase (LASY)
Article Snippet: RNA from tissue samples was isolated using tissue-specific kits from Qiagen. .. Monocyte chemoattractant protein-1 (MCP-1) enzyme-linked immunosorbent assay (ELISA) was carried out using the Quantikine Human MCP-1 kit as described by the manufacturer (R&D Systems). ..

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CCL2 expression is elevated in malignant pleural effusions and osimertinib-resistant cells. (A) Relative CCL2 mRNA expression in primary tumor cells isolated from malignant pleural effusions (MPEs) of lung adenocarcinoma patients harboring EGFR mutations. Samples were obtained from treatment-naïve patients (n = 26), patients with acquired resistance to osimertinib (n = 16), and patients with resistance to first- or second-generation EGFR-TKIs (gefitinib, erlotinib, or afatinib; n = 21). Each data point represents an independent biological sample. Data are presented as median with interquartile range. Statistical comparisons were performed using the Mann–Whitney U test; effect size (rank-biserial correlation) is shown where applicable. (B, C) Quantitative RT-PCR analysis of CCL2 mRNA expression in parental and resistant cell lines. Data represent the mean ± SD from three independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t-test ). (D, E) Secreted CCL2 protein levels measured by ELISA in the conditioned media of the same cell lines. Data represent the mean ± SD from three independent biological experiments (***p < 0.001, Student’s t-test ).

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: CCL2 expression is elevated in malignant pleural effusions and osimertinib-resistant cells. (A) Relative CCL2 mRNA expression in primary tumor cells isolated from malignant pleural effusions (MPEs) of lung adenocarcinoma patients harboring EGFR mutations. Samples were obtained from treatment-naïve patients (n = 26), patients with acquired resistance to osimertinib (n = 16), and patients with resistance to first- or second-generation EGFR-TKIs (gefitinib, erlotinib, or afatinib; n = 21). Each data point represents an independent biological sample. Data are presented as median with interquartile range. Statistical comparisons were performed using the Mann–Whitney U test; effect size (rank-biserial correlation) is shown where applicable. (B, C) Quantitative RT-PCR analysis of CCL2 mRNA expression in parental and resistant cell lines. Data represent the mean ± SD from three independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t-test ). (D, E) Secreted CCL2 protein levels measured by ELISA in the conditioned media of the same cell lines. Data represent the mean ± SD from three independent biological experiments (***p < 0.001, Student’s t-test ).

Article Snippet: We used 24-hour cell-conditioned media that were controlled for cell number and media volume to detect CCL2 using human CCL2 enzyme-linked immunosorbent assay (ELISA) kits (DCP00, R&D Systems) according to the manufacturer’s instructions.

Techniques: Expressing, Isolation, MANN-WHITNEY, Quantitative RT-PCR, Enzyme-linked Immunosorbent Assay

Gain- and loss-of-function analyses reveal that CCL2 regulates osimertinib resistance by suppressing apoptosis. (A) CCL2 mRNA levels in HCC827-mock and HCC827-CCL2 cells were quantified by RT-qPCR (***p < 0.001). (B) Cell viability after 48 h of osimertinib treatment was assessed by MTT assay. DMSO-treated cells were normalized to 100%. Data represent the mean ± SD from four independent experiments, each performed in triplicate (***p < 0.001, Student’s t-test). (C) CCL2 mRNA levels in HCC827/gef cells transfected with CCL2 siRNA were quantified by RT-qPCR. Data represent the mean ± SD from three independent biological replicates (***p < 0.001, Student’s t-test). (D) Cell viability after 72 h of osimertinib treatment was measured by MTT assay. (E) CCL2 mRNA levels in H1975/AZD-18 cells transfected with CCL2 siRNA were quantified by RT-qPCR. Data represent the mean ± SD from three independent biological replicates (***p < 0.001, Student’s t-test). (F) Osimertinib sensitivity in si-CCL2 cells was determined by MTT assay. Data represent the mean ± SD from three independent biological replicates (***p < 0.001, Student’s t-test). (G) Caspase-9 activity in HCC827-CCL2 cells after osimertinib treatment (***p < 0.001). (H) Caspase-9 activity in CCL2-knockdown cells following 500 nM osimertinib exposure for 24 h (**p < 0.01; ***p < 0.001, Student’s t-test). (I) Flow cytometry analysis of apoptosis (Annexin V/PI) in HCC827/gef cells. The bar chart displays the percentage of apoptotic cells derived from three independent experiments (**p < 0.01 compared with vehicle control, Student’s t-test ). (J, K) Western blot analysis of cleaved PARP and α-tubulin in CCL2-knockdown cells treated with osimertinib. Representative blots are shown from three independent experiments. (L) Cell viability of H1975/AZD-18 cells treated with osimertinib in the presence or absence of the CCL2-neutralizing antibody carlumab was assessed by MTT assay. Data represent the mean ± SD from three independent experiments (***p < 0.001, Student’s t-test).

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: Gain- and loss-of-function analyses reveal that CCL2 regulates osimertinib resistance by suppressing apoptosis. (A) CCL2 mRNA levels in HCC827-mock and HCC827-CCL2 cells were quantified by RT-qPCR (***p < 0.001). (B) Cell viability after 48 h of osimertinib treatment was assessed by MTT assay. DMSO-treated cells were normalized to 100%. Data represent the mean ± SD from four independent experiments, each performed in triplicate (***p < 0.001, Student’s t-test). (C) CCL2 mRNA levels in HCC827/gef cells transfected with CCL2 siRNA were quantified by RT-qPCR. Data represent the mean ± SD from three independent biological replicates (***p < 0.001, Student’s t-test). (D) Cell viability after 72 h of osimertinib treatment was measured by MTT assay. (E) CCL2 mRNA levels in H1975/AZD-18 cells transfected with CCL2 siRNA were quantified by RT-qPCR. Data represent the mean ± SD from three independent biological replicates (***p < 0.001, Student’s t-test). (F) Osimertinib sensitivity in si-CCL2 cells was determined by MTT assay. Data represent the mean ± SD from three independent biological replicates (***p < 0.001, Student’s t-test). (G) Caspase-9 activity in HCC827-CCL2 cells after osimertinib treatment (***p < 0.001). (H) Caspase-9 activity in CCL2-knockdown cells following 500 nM osimertinib exposure for 24 h (**p < 0.01; ***p < 0.001, Student’s t-test). (I) Flow cytometry analysis of apoptosis (Annexin V/PI) in HCC827/gef cells. The bar chart displays the percentage of apoptotic cells derived from three independent experiments (**p < 0.01 compared with vehicle control, Student’s t-test ). (J, K) Western blot analysis of cleaved PARP and α-tubulin in CCL2-knockdown cells treated with osimertinib. Representative blots are shown from three independent experiments. (L) Cell viability of H1975/AZD-18 cells treated with osimertinib in the presence or absence of the CCL2-neutralizing antibody carlumab was assessed by MTT assay. Data represent the mean ± SD from three independent experiments (***p < 0.001, Student’s t-test).

Techniques: Quantitative RT-PCR, MTT Assay, Transfection, Activity Assay, Knockdown, Flow Cytometry, Derivative Assay, Control, Western Blot

CCL2 overexpression attenuates the antitumor efficacy of osimertinib and shortens survival in xenograft models. (A) Growth curves of HCC827-CCL2 and HCC827-mock xenografts in SCID mice (n = 6 per group). Tumor volumes were measured every 4 days and expressed as mean ± standard error (SE). ns, not significant. (B) Kaplan–Meier survival curves comparing mice bearing HCC827-CCL2 and mock xenografts. No significant difference was observed between groups (log-rank test, p > 0.05). (C) Tumor growth of mice treated with osimertinib (0.5 mg/kg/day) for 32 days (n = 6 per group). Data are presented as mean ± SE (*p < 0.05, Student’s t-test ). (D) Kaplan–Meier survival analysis of osimertinib-treated xenograft-bearing mice (HCC827-CCL2 vs mock). Survival was defined by tumor volume <400 mm³. Statistical significance was determined by the log-rank (Mantel–Cox) test (p = 0.019).

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: CCL2 overexpression attenuates the antitumor efficacy of osimertinib and shortens survival in xenograft models. (A) Growth curves of HCC827-CCL2 and HCC827-mock xenografts in SCID mice (n = 6 per group). Tumor volumes were measured every 4 days and expressed as mean ± standard error (SE). ns, not significant. (B) Kaplan–Meier survival curves comparing mice bearing HCC827-CCL2 and mock xenografts. No significant difference was observed between groups (log-rank test, p > 0.05). (C) Tumor growth of mice treated with osimertinib (0.5 mg/kg/day) for 32 days (n = 6 per group). Data are presented as mean ± SE (*p < 0.05, Student’s t-test ). (D) Kaplan–Meier survival analysis of osimertinib-treated xenograft-bearing mice (HCC827-CCL2 vs mock). Survival was defined by tumor volume <400 mm³. Statistical significance was determined by the log-rank (Mantel–Cox) test (p = 0.019).

Techniques: Over Expression

CCL2 activates STAT3 and ERK. (A) Spearman’s correlation coefficients were calculated between CCL2 expression and the enrichment scores of MSigDB Hallmark gene sets derived from TCGA-LUAD transcriptomes. Only significantly correlated pathways (FDR < 0.01) are shown. (B) Western blot analysis of phosphorylated STAT3 and ERK1/2 in HCC827-CCL2 cells compared with vector control. CCL2 overexpression led to increased phosphorylation of STAT3 and ERK1/2, while p-AKT levels remained unchanged. (C) Phosphorylated STAT3 and ERK1/2 in HCC827/gef-si-CCL2 cells compared with control transfectants. Knockdown of CCL2 reduced p-STAT3 and p-ERK1/2 levels. α-tubulin served as the loading control. Representative blots are shown from three independent biological experiments.

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: CCL2 activates STAT3 and ERK. (A) Spearman’s correlation coefficients were calculated between CCL2 expression and the enrichment scores of MSigDB Hallmark gene sets derived from TCGA-LUAD transcriptomes. Only significantly correlated pathways (FDR < 0.01) are shown. (B) Western blot analysis of phosphorylated STAT3 and ERK1/2 in HCC827-CCL2 cells compared with vector control. CCL2 overexpression led to increased phosphorylation of STAT3 and ERK1/2, while p-AKT levels remained unchanged. (C) Phosphorylated STAT3 and ERK1/2 in HCC827/gef-si-CCL2 cells compared with control transfectants. Knockdown of CCL2 reduced p-STAT3 and p-ERK1/2 levels. α-tubulin served as the loading control. Representative blots are shown from three independent biological experiments.

Techniques: Expressing, Derivative Assay, Western Blot, Plasmid Preparation, Control, Over Expression, Phospho-proteomics, Knockdown

Targeting ZEB1 reverses osimertinib resistance in lung cancer cells. (A) Western blot analysis of EMT-related transcription factors in HCC827-CCL2 overexpression cells compared with vector control. ZEB1 expression levels increased upon CCL2 overexpression. Representative blots are shown from three independent experiments. (B) RT-qPCR and (C) Western blot analysis confirming ZEB1 knockdown efficiency in HCC827-CCL2 cells. Data represent the mean ± SD from three independent biological experiments (***p < 0.001, Student’s t -test). (D) MTT assay showing that ZEB1 knockdown restored osimertinib sensitivity in HCC827-CCL2 cells. Data represent the mean ± SD from four independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t -test). (E) RT-qPCR and (F) Western blot analysis confirming ZEB1 knockdown efficiency in H1975/AZD-18 cells. Data represent the mean ± SD from three independent biological experiments (***p < 0.001, Student’s t -test). (G) MTT assay showing that ZEB1 knockdown restored osimertinib sensitivity in H1975/AZD-18 cells. Data represent the mean ± SD from four independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t -test).

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: Targeting ZEB1 reverses osimertinib resistance in lung cancer cells. (A) Western blot analysis of EMT-related transcription factors in HCC827-CCL2 overexpression cells compared with vector control. ZEB1 expression levels increased upon CCL2 overexpression. Representative blots are shown from three independent experiments. (B) RT-qPCR and (C) Western blot analysis confirming ZEB1 knockdown efficiency in HCC827-CCL2 cells. Data represent the mean ± SD from three independent biological experiments (***p < 0.001, Student’s t -test). (D) MTT assay showing that ZEB1 knockdown restored osimertinib sensitivity in HCC827-CCL2 cells. Data represent the mean ± SD from four independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t -test). (E) RT-qPCR and (F) Western blot analysis confirming ZEB1 knockdown efficiency in H1975/AZD-18 cells. Data represent the mean ± SD from three independent biological experiments (***p < 0.001, Student’s t -test). (G) MTT assay showing that ZEB1 knockdown restored osimertinib sensitivity in H1975/AZD-18 cells. Data represent the mean ± SD from four independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t -test).

Techniques: Western Blot, Over Expression, Plasmid Preparation, Control, Expressing, Quantitative RT-PCR, Knockdown, MTT Assay

Blocking CCR2–STAT3/ERK signaling restores osimertinib sensitivity (A) Western blot analysis of CCR2 expression in HCC827-CCL2 cells after transfection with CCR2 siRNA. Representative blots are shown from three independent biological experiments. (B) MTT assay showing reduced viability of HCC827-CCL2-si-CCR2 cells treated with osimertinib (48 h). Data represent the mean ± SD from three independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t-test ). (C) Caspase-9 activity increased in CCR2-knockdown cells upon osimertinib treatment, measured by luminescent Caspase-Glo 9 assay. Data represent the mean ± SD from three independent experiments (***p < 0.001 vs. si-scramble, Student’s t-test ). (D) Western blot analysis of downstream signaling proteins (p-STAT3, p-ERK1/2, ZEB1) in HCC827-CCL2 cells treated with CCR2 antagonist INCB3344. Representative blots are shown from three independent experiments. (E) Combined treatment with osimertinib and INCB3344 decreased cell viability in HCC827-CCL2 cells (MTT assay). Data represent the mean ± SD from three independent biological replicates (*p < 0.05, Student’s t-test ). (F) INCB3344 enhanced caspase-9 activity upon osimertinib treatment. Data represent the mean ± SD from three independent biological experiments (**p < 0.01, Student’s t-test ). (G) HCC827-CCL2 cells treated with STAT3 inhibitor (S3I201, 40 μM, 24 h) were analyzed by Western blot for p-STAT3, p-ERK1/2, and ZEB1. Representative blots are shown from three independent experiments. (H) MTT assay showing that STAT3 inhibition sensitized HCC827-CCL2 cells to osimertinib treatment. Data represent the mean ± SD from three independent experiments (**p < 0.01, Student’s t-test ). (I) Tumor volume of H1975/AZD-18 xenografts treated with vehicle, osimertinib (1mg/kg/day), S3I201 (5mg/kg/2day), or a combination of both drugs for 16days (n = 5 in each subgroup). Data are presented as mean ± SE (*p < 0.05, Student’s t-test) . (J) Chromatin immunoprecipitation (ChIP) assay demonstrating STAT3 binding to the ZEB1 promoter in H1975/AZD-18 cells. Enrichment of ZEB1 promoter fragments was quantified by qPCR and normalized to IgG control. Data represent the mean ± SD from three independent experiments (*p < 0.05, Student’s t-test). (K) The expression of p-STAT3, p-ERK1/2, STAT3, ERK, and ZEB1 in HCC827-CCL2 cells with ERK inhibitor selumetinib was measured using Western blot analysis. Representative blots are shown from three independent experiments. (L) HCC872-CCL2 cells were treated with osimertinib and selumetinib treatment alone or in combination for 48 h; cell viability was determined using MTT assays. Data represent the mean ± SD from three independent experiments (**p < 0.001, Student’s t-test ).

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: Blocking CCR2–STAT3/ERK signaling restores osimertinib sensitivity (A) Western blot analysis of CCR2 expression in HCC827-CCL2 cells after transfection with CCR2 siRNA. Representative blots are shown from three independent biological experiments. (B) MTT assay showing reduced viability of HCC827-CCL2-si-CCR2 cells treated with osimertinib (48 h). Data represent the mean ± SD from three independent biological experiments, each performed in triplicate (***p < 0.001, Student’s t-test ). (C) Caspase-9 activity increased in CCR2-knockdown cells upon osimertinib treatment, measured by luminescent Caspase-Glo 9 assay. Data represent the mean ± SD from three independent experiments (***p < 0.001 vs. si-scramble, Student’s t-test ). (D) Western blot analysis of downstream signaling proteins (p-STAT3, p-ERK1/2, ZEB1) in HCC827-CCL2 cells treated with CCR2 antagonist INCB3344. Representative blots are shown from three independent experiments. (E) Combined treatment with osimertinib and INCB3344 decreased cell viability in HCC827-CCL2 cells (MTT assay). Data represent the mean ± SD from three independent biological replicates (*p < 0.05, Student’s t-test ). (F) INCB3344 enhanced caspase-9 activity upon osimertinib treatment. Data represent the mean ± SD from three independent biological experiments (**p < 0.01, Student’s t-test ). (G) HCC827-CCL2 cells treated with STAT3 inhibitor (S3I201, 40 μM, 24 h) were analyzed by Western blot for p-STAT3, p-ERK1/2, and ZEB1. Representative blots are shown from three independent experiments. (H) MTT assay showing that STAT3 inhibition sensitized HCC827-CCL2 cells to osimertinib treatment. Data represent the mean ± SD from three independent experiments (**p < 0.01, Student’s t-test ). (I) Tumor volume of H1975/AZD-18 xenografts treated with vehicle, osimertinib (1mg/kg/day), S3I201 (5mg/kg/2day), or a combination of both drugs for 16days (n = 5 in each subgroup). Data are presented as mean ± SE (*p < 0.05, Student’s t-test) . (J) Chromatin immunoprecipitation (ChIP) assay demonstrating STAT3 binding to the ZEB1 promoter in H1975/AZD-18 cells. Enrichment of ZEB1 promoter fragments was quantified by qPCR and normalized to IgG control. Data represent the mean ± SD from three independent experiments (*p < 0.05, Student’s t-test). (K) The expression of p-STAT3, p-ERK1/2, STAT3, ERK, and ZEB1 in HCC827-CCL2 cells with ERK inhibitor selumetinib was measured using Western blot analysis. Representative blots are shown from three independent experiments. (L) HCC872-CCL2 cells were treated with osimertinib and selumetinib treatment alone or in combination for 48 h; cell viability was determined using MTT assays. Data represent the mean ± SD from three independent experiments (**p < 0.001, Student’s t-test ).

Techniques: Blocking Assay, Western Blot, Expressing, Transfection, MTT Assay, Activity Assay, Knockdown, Inhibition, Chromatin Immunoprecipitation, Binding Assay, Control

Model of the regulatory signaling networks of CCL2-CCR2-STAT3/ERK-ZEB1 in osimertinib resistance.

Journal: Frontiers in Oncology

Article Title: The STAT3–ZEB1 axis contributes to CCL2-mediated resistance to osimertinib in lung cancer

doi: 10.3389/fonc.2026.1699471

Figure Lengend Snippet: Model of the regulatory signaling networks of CCL2-CCR2-STAT3/ERK-ZEB1 in osimertinib resistance.

Techniques:

(A) Summary of secreted protein expression in VPC conditioned media by ELISA. Data is mean concentration (pg/mL) ± standard deviation in VPC and extended culture VPC (EXT VPC). *p<0.05 vs. VPC, Student’s t -test. (B) Endothelial cytoprotection indicated as live HUVEC counts following co-culture with VPC (1:2 HUVEC:VPC) and AnnexinV/7-AAD staining. Data is mean ± standard deviation, n=17 for ctrl & GM, n=16 for VPC, n=15 for EXT VPC, and n=16 for HUVEC and represent independent biological repeats. GM=complete Vasculife growth media; *p<0.05 vs ctrl; One-Way ANOVA, Tukey’s post-hoc. (C) Normalized myocyte survival with VPC conditioned media after 7 days in 1% hypoxia and serum starvation; *p<0.05 vs ctrl; One-Way ANOVA, Tukey’s post-hoc. N=3 for PBS, ctrl, and complete Vasculife growth media (GM), n=2 for HUVEC, n=8 for VPC and represent independent biological repeats. Data is mean ± SEM (D) Tube stabilization of pre-formed vascular networks by VPC quantified by total tubes and total branchpoints of both GFP-HUVEC+ and phase contrast images. Note phase contrast images demonstrate incorporation of VPCs into the HUVEC network. Data is mean ± SEM. (E) IL6 secretion 48-hours after co-culture of VPC with THP1 monocytes (1:2 ratio) with 20ng/mL IFNγ stimulation as pg/mL/ug total protein. *p<0.05 vs ctrl; One-Way ANOVA, Tukey’s post-hoc, n=3 (naïve), n=3 (ctrl, THP1 + IFN (no VPC)), n=9 (VPC+THP1+IFN) biological replicates

Journal: bioRxiv

Article Title: Scalable Generation of Universal hiPSC-Derived Vascular Progenitor Cells for Safe and Sustained Revascularization in Chronic Limb-Threatening Ischemia

doi: 10.64898/2026.01.16.699995

Figure Lengend Snippet: (A) Summary of secreted protein expression in VPC conditioned media by ELISA. Data is mean concentration (pg/mL) ± standard deviation in VPC and extended culture VPC (EXT VPC). *p<0.05 vs. VPC, Student’s t -test. (B) Endothelial cytoprotection indicated as live HUVEC counts following co-culture with VPC (1:2 HUVEC:VPC) and AnnexinV/7-AAD staining. Data is mean ± standard deviation, n=17 for ctrl & GM, n=16 for VPC, n=15 for EXT VPC, and n=16 for HUVEC and represent independent biological repeats. GM=complete Vasculife growth media; *p<0.05 vs ctrl; One-Way ANOVA, Tukey’s post-hoc. (C) Normalized myocyte survival with VPC conditioned media after 7 days in 1% hypoxia and serum starvation; *p<0.05 vs ctrl; One-Way ANOVA, Tukey’s post-hoc. N=3 for PBS, ctrl, and complete Vasculife growth media (GM), n=2 for HUVEC, n=8 for VPC and represent independent biological repeats. Data is mean ± SEM (D) Tube stabilization of pre-formed vascular networks by VPC quantified by total tubes and total branchpoints of both GFP-HUVEC+ and phase contrast images. Note phase contrast images demonstrate incorporation of VPCs into the HUVEC network. Data is mean ± SEM. (E) IL6 secretion 48-hours after co-culture of VPC with THP1 monocytes (1:2 ratio) with 20ng/mL IFNγ stimulation as pg/mL/ug total protein. *p<0.05 vs ctrl; One-Way ANOVA, Tukey’s post-hoc, n=3 (naïve), n=3 (ctrl, THP1 + IFN (no VPC)), n=9 (VPC+THP1+IFN) biological replicates

Article Snippet: Media was collected, centrifuged to remove any dead cells, and supernatants were analyzed using the Angiogenesis Array G1000 (Cat. No AAH-ANG-G1000-4) which was scanned and quantified at RayBioTech or with the following human Quantikine ELISA (R&D Systems) kits according to manufacturer’s instructions: HGF (DHG00B), CCL2/MCP-1 (CDP00), ANGPT2 (DANG20), ANGPT1 (DANG10), FGF2/bFGF (DFB50), CXCL12/SDF1 (DSA00), FST/follistatin (DFN00), ANG/angiogenin (DNA00), MMP2 (DMP2F0), EGF (DEG00) and ANGPTL4 (Invitrogen, EHANGPTL4).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Concentration Assay, Standard Deviation, Co-Culture Assay, Staining

Differential serum levels of key pyroptosis-related cytokines among healthy controls, non-oGVHD patients, and oGVHD patients. (A) Serum NLRP3 levels. (B) Serum TLR4 levels. (C) Serum CCL2 levels. (D) Serum IL-18 levels. (E) Serum IL-6 levels. (F) Serum TNF-α levels. Data are presented as mean ± standard deviation (SD). Comparisons among the three groups were performed using one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test for normally distributed data, or Kruskal–Wallis H -test followed by Dunn’s post hoc test for non-normally distributed data, as appropriate. Significant levels; ** p < 0.01; **** p < 0.0001. p < 0.05 was considered statistically significant.

Journal: Journal of Inflammation Research

Article Title: Serum Pyroptosis-Related Cytokines as Biomarkers for Diagnostic Assessment and Risk Stratification of Ocular Graft-versus-Host Disease: A Case-Control Study

doi: 10.2147/JIR.S552170

Figure Lengend Snippet: Differential serum levels of key pyroptosis-related cytokines among healthy controls, non-oGVHD patients, and oGVHD patients. (A) Serum NLRP3 levels. (B) Serum TLR4 levels. (C) Serum CCL2 levels. (D) Serum IL-18 levels. (E) Serum IL-6 levels. (F) Serum TNF-α levels. Data are presented as mean ± standard deviation (SD). Comparisons among the three groups were performed using one-way analysis of variance (ANOVA) followed by Tukey’s post hoc test for normally distributed data, or Kruskal–Wallis H -test followed by Dunn’s post hoc test for non-normally distributed data, as appropriate. Significant levels; ** p < 0.01; **** p < 0.0001. p < 0.05 was considered statistically significant.

Article Snippet: The ELISA kits used in this study were as follows:NLRP3 (ab274401, Abcam, UK), TLR4 (EH460RB, Thermo Fisher Scientific, USA), CCL2 (DCP00, R&D Systems, USA), IL-18 (7620, MBL International, Japan), IL-6 (KHC0061, Thermo Fisher Scientific, USA), TNF-α (NBP1-91170, Novus Biologicals, USA), CXCL2 (OKCD07517, Aviva Systems Biology, USA), STAT1 (CBA034, Merck Millipore, USA), STAT2 (NBP3-40521, Novus Biologicals, USA), JAK1 (MBS2021168, MyBioSource, USA), and AKT2 (ab208986, Abcam, UK).

Techniques: Standard Deviation

Receiver operating characteristic (ROC) curves depicting the diagnostic performance of individual inflammatory biomarkers (NLRP3, TLR4, CCL2, IL-18, and IL-6) and their combination for predicting oGVHD. The multivariate model achieved the highest diagnostic accuracy, with an area under the curve (AUC) of 0.953. The diagonal line represents the reference (non-informative) classifier with an AUC of 0.5.

Journal: Journal of Inflammation Research

Article Title: Serum Pyroptosis-Related Cytokines as Biomarkers for Diagnostic Assessment and Risk Stratification of Ocular Graft-versus-Host Disease: A Case-Control Study

doi: 10.2147/JIR.S552170

Figure Lengend Snippet: Receiver operating characteristic (ROC) curves depicting the diagnostic performance of individual inflammatory biomarkers (NLRP3, TLR4, CCL2, IL-18, and IL-6) and their combination for predicting oGVHD. The multivariate model achieved the highest diagnostic accuracy, with an area under the curve (AUC) of 0.953. The diagonal line represents the reference (non-informative) classifier with an AUC of 0.5.

Techniques: Diagnostic Assay

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