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R&D Systems respective quantikine elisa kits

a Images of splinted db/db mouse wounds at day 10 post wounding. b Quantification of migrating epithelial tongues from splinted db/db mouse wounds [Error bars correspond to standard deviations from 4 biological specimens with statistical significance assessed using paired 2-way ANOVA followed by Tukey’s multiple comparison testing, * p < 0.05, ** p < 0.01, **** p < 0.0001]. c IHC staining and d quantification of CD31 + cells/mm 2 demonstrating increased number blood vessels with HβCD + EGF treatment [Error bars correspond to standard deviations from four biological specimens with statistical significance assessed using paired student t -test, **** p < 0.0001] (E-epidermis, D-dermis; scale bar = 50 µm). d <t>ELISA</t> demonstrating increased levels of VEGF in splinted db/db mouse wounds upon incorporation of growth factors into HβCD hydrogels [Error bars correspond to standard deviations from four biological specimens with statistical significance assessed using paired 2-way ANOVA followed by Tukey’s multiple comparison testing, * p < 0.05, ** p < 0.01, **** p < 0.0001]. (scale bar = 50 µm).

Respective Quantikine Elisa Kits, supplied by R&D Systems, used in various techniques. Bioz Stars score: 95/100, based on 113 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 113 article reviews

respective quantikine elisa kits - by Bioz Stars, 2026-07

95/100 stars

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1) Product Images from "Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing"

Article Title: Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing

Journal: NPJ Regenerative Medicine

doi: 10.1038/s41536-025-00431-0

Figure Legend Snippet: a Images of splinted db/db mouse wounds at day 10 post wounding. b Quantification of migrating epithelial tongues from splinted db/db mouse wounds [Error bars correspond to standard deviations from 4 biological specimens with statistical significance assessed using paired 2-way ANOVA followed by Tukey’s multiple comparison testing, * p < 0.05, ** p < 0.01, **** p < 0.0001]. c IHC staining and d quantification of CD31 + cells/mm 2 demonstrating increased number blood vessels with HβCD + EGF treatment [Error bars correspond to standard deviations from four biological specimens with statistical significance assessed using paired student t -test, **** p < 0.0001] (E-epidermis, D-dermis; scale bar = 50 µm). d ELISA demonstrating increased levels of VEGF in splinted db/db mouse wounds upon incorporation of growth factors into HβCD hydrogels [Error bars correspond to standard deviations from four biological specimens with statistical significance assessed using paired 2-way ANOVA followed by Tukey’s multiple comparison testing, * p < 0.05, ** p < 0.01, **** p < 0.0001]. (scale bar = 50 µm).

Techniques Used: Comparison, Immunohistochemistry, Enzyme-linked Immunosorbent Assay

Image Search Results

Journal: NPJ Regenerative Medicine

Article Title: Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing

doi: 10.1038/s41536-025-00431-0

Figure Lengend Snippet: a Images of splinted db/db mouse wounds at day 10 post wounding. b Quantification of migrating epithelial tongues from splinted db/db mouse wounds [Error bars correspond to standard deviations from 4 biological specimens with statistical significance assessed using paired 2-way ANOVA followed by Tukey’s multiple comparison testing, * p < 0.05, ** p < 0.01, **** p < 0.0001]. c IHC staining and d quantification of CD31 + cells/mm 2 demonstrating increased number blood vessels with HβCD + EGF treatment [Error bars correspond to standard deviations from four biological specimens with statistical significance assessed using paired student t -test, **** p < 0.0001] (E-epidermis, D-dermis; scale bar = 50 µm). d ELISA demonstrating increased levels of VEGF in splinted db/db mouse wounds upon incorporation of growth factors into HβCD hydrogels [Error bars correspond to standard deviations from four biological specimens with statistical significance assessed using paired 2-way ANOVA followed by Tukey’s multiple comparison testing, * p < 0.05, ** p < 0.01, **** p < 0.0001]. (scale bar = 50 µm).

Article Snippet: For determination of growth factor release from the hydrogels, gelatin hydrogels were loaded onto 0.4 μm PET membranes within a 24 well plate, submerged in PBS, and growth factor release quantified at 0, 12, 24, 48, 96 and 120 h using respective Quantikine ELISA kits (R&D Systems, DEG00 for EGF, DBB00 for PDGF-BB, and DVE00 for VEGF).

Techniques: Comparison, Immunohistochemistry, Enzyme-linked Immunosorbent Assay

(A) Uniform manifold approximation and projection (UMAP) demonstrating clustering of detectable cell populations based on single-cell transcriptional profiling. Each dot represents a single cell with color corresponding to cell type (CMP, common myeloid progenitor; DC, dendritic cell; GMP, granulocyte monocyte progenitor; HSC, hematopoietic stem cell; MEP, megakaryocyte erythroid progenitor). (B) Hierarchical clustering of detectable cell populations based on transcriptional profiling. Each hashmark represents a single cell. Colors represent normalized scores. (C) Pie chart depicting percent frequency of classifiable hematopoietic cell populations identified by scRNA-Seq across all 7 patients.(CMP, common myeloid progenitor; GMP, granulocyte monocyte progenitor; HSC, hematopoietic stem cell; MEP, megakaryocyte erythroid progenitor). (D) Percent frequency of detectable cell populations identified by scRNA-Seq per patient. (E) UMAPs of common myeloid progenitor (CMP; left panel) and granulocyte-monocyte progenitor (GMP; right panel) populations colored by patient (ET, essential thrombocythemia; PV, polycythemia vera; MF, myelofibrosis). Each dot represents a single cell. (F) Violin plots showing relative expression of CXCR2-mediated cytokines CXCL8 (left panel), CXCL2 (middle panel), and CXCL3 (right panel) in CMPs of individual MPN patients by scRNA-Seq. Each dot represents a single cell.

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Uniform manifold approximation and projection (UMAP) demonstrating clustering of detectable cell populations based on single-cell transcriptional profiling. Each dot represents a single cell with color corresponding to cell type (CMP, common myeloid progenitor; DC, dendritic cell; GMP, granulocyte monocyte progenitor; HSC, hematopoietic stem cell; MEP, megakaryocyte erythroid progenitor). (B) Hierarchical clustering of detectable cell populations based on transcriptional profiling. Each hashmark represents a single cell. Colors represent normalized scores. (C) Pie chart depicting percent frequency of classifiable hematopoietic cell populations identified by scRNA-Seq across all 7 patients.(CMP, common myeloid progenitor; GMP, granulocyte monocyte progenitor; HSC, hematopoietic stem cell; MEP, megakaryocyte erythroid progenitor). (D) Percent frequency of detectable cell populations identified by scRNA-Seq per patient. (E) UMAPs of common myeloid progenitor (CMP; left panel) and granulocyte-monocyte progenitor (GMP; right panel) populations colored by patient (ET, essential thrombocythemia; PV, polycythemia vera; MF, myelofibrosis). Each dot represents a single cell. (F) Violin plots showing relative expression of CXCR2-mediated cytokines CXCL8 (left panel), CXCL2 (middle panel), and CXCL3 (right panel) in CMPs of individual MPN patients by scRNA-Seq. Each dot represents a single cell.

Article Snippet: After 3 days of co-cultivation, the media were collected and analyzed for secretion of CXCL8 and VEGF using respective ELISA kits (CXCL8: Cat# D8000C, R&DSystem; VEGF: Cat# DVE00, R&DSystem); the results were then normalized by cell number.

Techniques: Expressing

$(A) Heatmap demonstrating frequency of individual cytokine secreting CD34+ cells detected among individual patients across MPN sub-types myelofibrosis (MF), polycythemia vera (PV), and essential thrombocythemia (ET) as a percentage of total cytokine-secreting cells (0% in gray to 100% in dark blue). Four cytokines presented: IL-6, MIP-1β, TNFα, and CXCL8. (B) Violin plot depicting correlation between MPN sub-type and percent fraction of CXCL8-only secreting cells as detected by single-cell cytokine analysis. *p<0.05. ***p<0.001. (C) Violin plot depicting correlation between bone marrow reticulin score (MF0-3) of MF patients and percent fraction of detected CXCL8-only secreting cells by single-cell cytokine analysis. (D) Receiver operator curve demonstrating association between percent CXCL8-only secreting cells and MF sub-type in comparison to PV/ET. A=area under the curve; P=p-value. (E) CXCL8 levels as detected by ELISA in isolated plasma from PV, ET, and MF MPN patients in comparison to healthy controls (CTRL). (CTRL N=8, PV N=16, ET N=16, MF N=35). *p<0.05. **p<0.01. Data shown represent mean ± SD. (F) Representative CXCL8 immunohistochemistry (IHC) of healthy donors and MF bone marrow (BM) and spleen (from N=0/4 healthy donors and N=8/15 MF patients). (G) Ratio of total cell output relative to untreated of cultured healthy donor (HD; light blue) vs. MF (dark blue) CD34+ cells in response to two exogenous CXCL8 doses (50ng, 100ng). *p<0.05. Representative of triplicate experiments from N=3 HD and N=6 MF samples. Data shown represent mean ± SD. (H) Percent of total CD34+ cells expressing CXCR1 (left panel) or CXCR2 (right panel) by flow cytometry of control (CTRL) vs. MF patients (N=13 CTRL, H=15 MF). *p<0.05. Data shown represent mean ± SD.$

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Heatmap demonstrating frequency of individual cytokine secreting CD34+ cells detected among individual patients across MPN sub-types myelofibrosis (MF), polycythemia vera (PV), and essential thrombocythemia (ET) as a percentage of total cytokine-secreting cells (0% in gray to 100% in dark blue). Four cytokines presented: IL-6, MIP-1β, TNFα, and CXCL8. (B) Violin plot depicting correlation between MPN sub-type and percent fraction of CXCL8-only secreting cells as detected by single-cell cytokine analysis. *p<0.05. ***p<0.001. (C) Violin plot depicting correlation between bone marrow reticulin score (MF0-3) of MF patients and percent fraction of detected CXCL8-only secreting cells by single-cell cytokine analysis. (D) Receiver operator curve demonstrating association between percent CXCL8-only secreting cells and MF sub-type in comparison to PV/ET. A=area under the curve; P=p-value. (E) CXCL8 levels as detected by ELISA in isolated plasma from PV, ET, and MF MPN patients in comparison to healthy controls (CTRL). (CTRL N=8, PV N=16, ET N=16, MF N=35). *p<0.05. **p<0.01. Data shown represent mean ± SD. (F) Representative CXCL8 immunohistochemistry (IHC) of healthy donors and MF bone marrow (BM) and spleen (from N=0/4 healthy donors and N=8/15 MF patients). (G) Ratio of total cell output relative to untreated of cultured healthy donor (HD; light blue) vs. MF (dark blue) CD34+ cells in response to two exogenous CXCL8 doses (50ng, 100ng). *p<0.05. Representative of triplicate experiments from N=3 HD and N=6 MF samples. Data shown represent mean ± SD. (H) Percent of total CD34+ cells expressing CXCR1 (left panel) or CXCR2 (right panel) by flow cytometry of control (CTRL) vs. MF patients (N=13 CTRL, H=15 MF). *p<0.05. Data shown represent mean ± SD.

Techniques: Enzyme-linked Immunosorbent Assay, Isolation, Immunohistochemistry, Cell Culture, Expressing, Flow Cytometry

$(A) Heatmap showing fraction of cells secreting single or >1 combined cytokines as detected by single-cell cytokine analysis for each individual patient evaluated (ET, essential thrombocythemia; PV, polycythemia vera; MF, myelofibrosis). Colors represent frequency among total cells (0% white; 100% dark blue). (B) Polyfunctionality index (PFI), or the fraction of multiple-secreting cytokine cell populations detected by single-cell cytokine arrays based on clinical MPN sub-type (EV, PV, or MF). ns=non-significant. (C) Box plots depicting correlation between MPN sub-type and percent fraction of RANTES-only secreting cells as detected by single-cell cytokine analysis. **p<0.01. ***p<0.001. ns=non-significant. (D) Linear correlation analysis of percent fraction of CXCL8-only secreting CD34+ cells detected by single-cell cytokine analysis and total white blood cell (WBC) count at time of sample collection.$

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Heatmap showing fraction of cells secreting single or >1 combined cytokines as detected by single-cell cytokine analysis for each individual patient evaluated (ET, essential thrombocythemia; PV, polycythemia vera; MF, myelofibrosis). Colors represent frequency among total cells (0% white; 100% dark blue). (B) Polyfunctionality index (PFI), or the fraction of multiple-secreting cytokine cell populations detected by single-cell cytokine arrays based on clinical MPN sub-type (EV, PV, or MF). ns=non-significant. (C) Box plots depicting correlation between MPN sub-type and percent fraction of RANTES-only secreting cells as detected by single-cell cytokine analysis. **p<0.01. ***p<0.001. ns=non-significant. (D) Linear correlation analysis of percent fraction of CXCL8-only secreting CD34+ cells detected by single-cell cytokine analysis and total white blood cell (WBC) count at time of sample collection.

Techniques:

$(A) Total levels of CXCL8 (left panel), VEGF (middle), and TGFβ (right) detected in conditioned media (CM) elicited from cultured healthy donor (light blue) vs. MF (dark blue) megakaryocytes (MK). *p<0.05. **p<0.01. ***p<0.001. Data shown represent mean ± SD. (B) Fold change of pro-inflammatory cytokine IL-6, TGFβ, CXCL8, and TGFβ gene expression by quantitative PCR from isolated MF MKs (dark blue) compared to healthy controls (light blue). P-values as indicated. (C) Ratio of total CD33+ cell output (left panel) and CD41+ cell output (right panel) relative to untreated of cultured healthy donor (light blue) vs. MF (dark blue) CD34+ cells in response to exogenous CXCL8 as detected by flow cytometry. *p<0.05. Data shown represent mean ± SD. (D) Ratio of granulocyte-macrophage progenitor (CFU-GM) colony output to control of cultured MF CD34+ cells in methylcellulose in response to increasing doses of exogenous CXCL8 stratified by degree of CXCR1/2 surface expression (“low:” <10% of cells; “high:” > 10% of cells) (E) Percentage of total MF CD34+ cells expressing CXCR1 (left panel) or CXCR2 (right panel) as detected by flow cytometry based on JAK2 V617F mutational status. **p-value <0.01. (F) Linear correlation analysis of percent fraction of CXCL8-only secreting CD34+ cells detected by single-cell cytokine analysis and JAK2 V617F variant allele fraction (VAF).$

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Total levels of CXCL8 (left panel), VEGF (middle), and TGFβ (right) detected in conditioned media (CM) elicited from cultured healthy donor (light blue) vs. MF (dark blue) megakaryocytes (MK). *p<0.05. **p<0.01. ***p<0.001. Data shown represent mean ± SD. (B) Fold change of pro-inflammatory cytokine IL-6, TGFβ, CXCL8, and TGFβ gene expression by quantitative PCR from isolated MF MKs (dark blue) compared to healthy controls (light blue). P-values as indicated. (C) Ratio of total CD33+ cell output (left panel) and CD41+ cell output (right panel) relative to untreated of cultured healthy donor (light blue) vs. MF (dark blue) CD34+ cells in response to exogenous CXCL8 as detected by flow cytometry. *p<0.05. Data shown represent mean ± SD. (D) Ratio of granulocyte-macrophage progenitor (CFU-GM) colony output to control of cultured MF CD34+ cells in methylcellulose in response to increasing doses of exogenous CXCL8 stratified by degree of CXCR1/2 surface expression (“low:” <10% of cells; “high:” > 10% of cells) (E) Percentage of total MF CD34+ cells expressing CXCR1 (left panel) or CXCR2 (right panel) as detected by flow cytometry based on JAK2 V617F mutational status. **p-value <0.01. (F) Linear correlation analysis of percent fraction of CXCL8-only secreting CD34+ cells detected by single-cell cytokine analysis and JAK2 V617F variant allele fraction (VAF).

Techniques: Cell Culture, Expressing, Real-time Polymerase Chain Reaction, Isolation, Flow Cytometry, Variant Assay

(A) Uniform manifold approximation and projection (UMAP) visualization of N=9 MPN patient samples (see ) available for gene expression (RNA-Seq) analysis. Each dot represents an individual patient. (Light blue represents CXCL8 “non-secretors;” dark blue represents CXCL8 “secretors” as identified by their single-cell cytokine secretion analysis). (B) Total number of differentially regulated genes (blue represents significantly down-regulated genes; red significantly up-regulated genes) of CXCL8 secretor vs. non-secretor MPN patients by a fold change cutoff of ± 2 and a FDR of 1%. (C) PCA plot demonstrating clustering of myelofibrosis patients segregated by CXCL8 expression levels and stratified by <20% and >80% from a publicly available microarray gene expression data set. Each dot represents an individual patient. Dark blue represents “ CXCL8 high” (>80%) MF patients; light blue represents “ CXCL8 low” (<20%) MF patients as based on their relative CXCL8 expression level. (D) Correlation analysis comparing the internal (MSKCC) RNA-Seq dataset to the publicly-available MF gene expression data set (as per Norfo et al). (E) Hierarchal clustering demonstrating differentially expressed genes in select MF patients stratified by CXCL8 expression level (light blue = CXCL8 low; dark blue = CXCL8 high). Blue, negative values; red, positive values. (F) Gene Set Enrichment Analysis (GSEA) demonstrating enriched pathways in “ CXCL8 high” vs. “ CXCL8 low” MF patients from the publicly-available dataset presented as normalized enrichment score (NES) by FDR q-value. (G) Representative GSEA plots demonstrating positive enrichment in pro-inflammatory signaling (TNFα via NF-κB) and myeloid cell/neutrophil activation gene sets in “ CXCL8 high” vs. “ CXCL8 low” MF patients from the publicly-available dataset.

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Uniform manifold approximation and projection (UMAP) visualization of N=9 MPN patient samples (see ) available for gene expression (RNA-Seq) analysis. Each dot represents an individual patient. (Light blue represents CXCL8 “non-secretors;” dark blue represents CXCL8 “secretors” as identified by their single-cell cytokine secretion analysis). (B) Total number of differentially regulated genes (blue represents significantly down-regulated genes; red significantly up-regulated genes) of CXCL8 secretor vs. non-secretor MPN patients by a fold change cutoff of ± 2 and a FDR of 1%. (C) PCA plot demonstrating clustering of myelofibrosis patients segregated by CXCL8 expression levels and stratified by <20% and >80% from a publicly available microarray gene expression data set. Each dot represents an individual patient. Dark blue represents “ CXCL8 high” (>80%) MF patients; light blue represents “ CXCL8 low” (<20%) MF patients as based on their relative CXCL8 expression level. (D) Correlation analysis comparing the internal (MSKCC) RNA-Seq dataset to the publicly-available MF gene expression data set (as per Norfo et al). (E) Hierarchal clustering demonstrating differentially expressed genes in select MF patients stratified by CXCL8 expression level (light blue = CXCL8 low; dark blue = CXCL8 high). Blue, negative values; red, positive values. (F) Gene Set Enrichment Analysis (GSEA) demonstrating enriched pathways in “ CXCL8 high” vs. “ CXCL8 low” MF patients from the publicly-available dataset presented as normalized enrichment score (NES) by FDR q-value. (G) Representative GSEA plots demonstrating positive enrichment in pro-inflammatory signaling (TNFα via NF-κB) and myeloid cell/neutrophil activation gene sets in “ CXCL8 high” vs. “ CXCL8 low” MF patients from the publicly-available dataset.

Techniques: Expressing, RNA Sequencing Assay, Microarray, Activation Assay

(A) Representative accessibility peaks at the CXCL8 locus of representative CXCL8-secretor vs. non-secretor MPN patients. (B) Volcano plot demonstrating most differentially expressed genes (DEGs) in CXCL8 secretor vs. non-secretor MPN patients by RNA-Seq. The significant events with an inclusion level >0.5 log fold change and an FDR-corrected P<0.0001 are shown in blue. (C) Gene Set Enrichment Analysis (GSEA) demonstrating enriched pathways of CXCL8 secretors vs. non-secretors by RNA-Seq plotted as normalized enrichment score (NES) by FDR q-value. (D) Optimized gene expression sub-network analysis from gene expression profiles showing key nodes enriched by RNA-Seq in CXCL8 secretor vs. non-secretor MPN patients. Additional information regarding the creation of sub-networks can be found in the STAR Methods. (E) Waterfall plot with integrated gene expression and chromatin accessibility showing most differentially regulated genes (represented as log2FoldChange) in CXCL8-secretors vs. non-secretors and their corresponding degree of changes in accessibility peaks (represented as log2FoldChange and -log10(padj), red, positive values; blue, negative values). (F) Tornado plot and heatmaps depicting accessibility at promoter regions of the top 500 leading edge genes in the TNFα via NF-κB gene set of CXCL8 non-secretor (N=2) vs. CXCL8 secretor (N=3) MPN patients .

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Representative accessibility peaks at the CXCL8 locus of representative CXCL8-secretor vs. non-secretor MPN patients. (B) Volcano plot demonstrating most differentially expressed genes (DEGs) in CXCL8 secretor vs. non-secretor MPN patients by RNA-Seq. The significant events with an inclusion level >0.5 log fold change and an FDR-corrected P<0.0001 are shown in blue. (C) Gene Set Enrichment Analysis (GSEA) demonstrating enriched pathways of CXCL8 secretors vs. non-secretors by RNA-Seq plotted as normalized enrichment score (NES) by FDR q-value. (D) Optimized gene expression sub-network analysis from gene expression profiles showing key nodes enriched by RNA-Seq in CXCL8 secretor vs. non-secretor MPN patients. Additional information regarding the creation of sub-networks can be found in the STAR Methods. (E) Waterfall plot with integrated gene expression and chromatin accessibility showing most differentially regulated genes (represented as log2FoldChange) in CXCL8-secretors vs. non-secretors and their corresponding degree of changes in accessibility peaks (represented as log2FoldChange and -log10(padj), red, positive values; blue, negative values). (F) Tornado plot and heatmaps depicting accessibility at promoter regions of the top 500 leading edge genes in the TNFα via NF-κB gene set of CXCL8 non-secretor (N=2) vs. CXCL8 secretor (N=3) MPN patients .

Techniques: RNA Sequencing Assay, Expressing

(A) Western blot analysis of canonical downstream Cxcr2 mediators in harvested murine bone marrow after 2 hours cultured with or without exogenous human CXCL8 for both Cxcr2 f/f ;Cre - wild-type (WT) and Cxcr2 f/f ;Cre + knock-out (KO) cells. (B) Schematic of experimental set up of the Cxcr2 -/- KO hMPL W515L transplant studies. (C) Confirmation of Cxcr2 loss on the surface of murine peripheral blood Mac1+Gr1+ cells from Cxcr2 f/f ;Cre + primary KO mice. ****p<0.0001. Data shown represent mean ± SEM. (D) Percent Mac1+Gr1+ mature neutrophil populations in peripheral blood of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice at time of sacrifice. ***p<0.001. Data shown represent mean ± SEM. (E) Representative flow cytometry plots demonstrating reduction in peripheral blood Mac1+Gr1+ mature neutrophil populations and corresponding detectable Cxcr2 surface expression of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice. (F) Bone marrow grade reticulin scores of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice. **p<0.01. Data shown represent mean ± SEM. (G) Representative hematoxylin and eosin (H&E) and reticulin images of spleen sections from Cxcr2 f/f ;Cre + KO vs. Cxcr2 f/f ;Cre - WT hMPL W515L mice. 20X magnification. (H) Percentage of CD41+ live cells as detected by flow cytometry in bone marrow of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice at time of sacrifice. **p<0.01. Data shown represent mean ± SEM. (I) Recorded bone marrow megakaryocyte number (MKs) per high powered field (HPF) observed (left panel) and representative H&E stains of bone marrow (right panel) from Cxcr2 f/f ;Cre + KO vs. Cxcr2 f/f ;Cre - WT hMPL W515L transplanted mice. N=4-7/arm. ****p<0.0001. 40X magnification. Data shown represent mean ± SEM.

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Western blot analysis of canonical downstream Cxcr2 mediators in harvested murine bone marrow after 2 hours cultured with or without exogenous human CXCL8 for both Cxcr2 f/f ;Cre - wild-type (WT) and Cxcr2 f/f ;Cre + knock-out (KO) cells. (B) Schematic of experimental set up of the Cxcr2 -/- KO hMPL W515L transplant studies. (C) Confirmation of Cxcr2 loss on the surface of murine peripheral blood Mac1+Gr1+ cells from Cxcr2 f/f ;Cre + primary KO mice. ****p<0.0001. Data shown represent mean ± SEM. (D) Percent Mac1+Gr1+ mature neutrophil populations in peripheral blood of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice at time of sacrifice. ***p<0.001. Data shown represent mean ± SEM. (E) Representative flow cytometry plots demonstrating reduction in peripheral blood Mac1+Gr1+ mature neutrophil populations and corresponding detectable Cxcr2 surface expression of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice. (F) Bone marrow grade reticulin scores of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice. **p<0.01. Data shown represent mean ± SEM. (G) Representative hematoxylin and eosin (H&E) and reticulin images of spleen sections from Cxcr2 f/f ;Cre + KO vs. Cxcr2 f/f ;Cre - WT hMPL W515L mice. 20X magnification. (H) Percentage of CD41+ live cells as detected by flow cytometry in bone marrow of Cxcr2 f/f ;Cre + vs. Cxcr2 f/f ;Cre - hMPL W515L transplanted mice at time of sacrifice. **p<0.01. Data shown represent mean ± SEM. (I) Recorded bone marrow megakaryocyte number (MKs) per high powered field (HPF) observed (left panel) and representative H&E stains of bone marrow (right panel) from Cxcr2 f/f ;Cre + KO vs. Cxcr2 f/f ;Cre - WT hMPL W515L transplanted mice. N=4-7/arm. ****p<0.0001. 40X magnification. Data shown represent mean ± SEM.

Techniques: Western Blot, Cell Culture, Knock-Out, Flow Cytometry, Expressing

(A) Representative Cxcl1, Cxcr1 and Cxcr2 immunohistochemistry of Gata1 low mice with active fibrosis in comparison to age-matched wild-type controls. N=6/arm. 40X magnification (quantitative data are presented in ). (B) White blood cell counts (WBC, K/uL), hematocrit levels (Hct, %), and platelet counts (PLT, K/uL) of Gata1 low mice treated with reparixin compared to mice treated with vehicle. N=3-4/condition. Data shown represent mean ± SEM. (C) Representative H&E and reticulin images of Gata1 low bone marrow treated with reparixin therapy compared to vehicle-treated mice. Magnification as indicated. (D) Colony forming unit (CFU) assay demonstrating total granulocyte-macrophage progenitor (CFU-GM) colony number relative to control of cultured healthy donor (HD; light blue) vs. MF (dark blue) CD34+ cells with exogenous CXCL8 ligand and response to the second-generation CXCR1/2 antagonist Ladarixin (10uM) in vitro . *p<0.05. **p<0.01. Representative of duplicate experiments from 5 HD and 13 individual MF cases. (E) Fold-change in detectable CXCL8 levels in conditioned media (CM) elicited by either healthy donor vs. MF megakaryocytes (MKs) with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD. (F) Total levels of CXCL8 in conditioned media (CM) of cultured stromal cells, either alone or together with healthy vs. MF megakaryocytes (MKs) with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD.

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Representative Cxcl1, Cxcr1 and Cxcr2 immunohistochemistry of Gata1 low mice with active fibrosis in comparison to age-matched wild-type controls. N=6/arm. 40X magnification (quantitative data are presented in ). (B) White blood cell counts (WBC, K/uL), hematocrit levels (Hct, %), and platelet counts (PLT, K/uL) of Gata1 low mice treated with reparixin compared to mice treated with vehicle. N=3-4/condition. Data shown represent mean ± SEM. (C) Representative H&E and reticulin images of Gata1 low bone marrow treated with reparixin therapy compared to vehicle-treated mice. Magnification as indicated. (D) Colony forming unit (CFU) assay demonstrating total granulocyte-macrophage progenitor (CFU-GM) colony number relative to control of cultured healthy donor (HD; light blue) vs. MF (dark blue) CD34+ cells with exogenous CXCL8 ligand and response to the second-generation CXCR1/2 antagonist Ladarixin (10uM) in vitro . *p<0.05. **p<0.01. Representative of duplicate experiments from 5 HD and 13 individual MF cases. (E) Fold-change in detectable CXCL8 levels in conditioned media (CM) elicited by either healthy donor vs. MF megakaryocytes (MKs) with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD. (F) Total levels of CXCL8 in conditioned media (CM) of cultured stromal cells, either alone or together with healthy vs. MF megakaryocytes (MKs) with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD.

Techniques: Immunohistochemistry, Colony-forming Unit Assay, Cell Culture, In Vitro

(A) Ratio of total CD33+ cell output relative to untreated of cultured healthy donor (HD; light blue) vs. myelofibrosis (MF; dark blue) CD34+ cells in response to exogenous CXCL8 doses (50ng vs. 100ng) with or without the CXCR1/2 inhibitor Ladarixin (10uM). *p<0.05. Data shown represent mean ± SD. (B) Ratio of total CD41+ cell output relative to untreated of cultured healthy donor (HD; light blue) vs. myelofibrosis (MF; dark blue) CD34+ cells in response to exogenous CXCL8 doses (50ng vs. 100ng) with or without the CXCR1/2 inhibitor Ladarixin (10uM). *p<0.05. Data shown represent mean ± SD. (C) Fold-change in detectable VEGF levels in conditioned media (CM) elicited by either healthy donor vs. MF megakaryocytes (MKs) with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD. (D) Total CXCL8 levels detected in conditioned media of various co-culture conditions (stromal cells alone +/- healthy donor or MF megakaryocytes [MK]). *p-value <0.05. Data shown represent mean ± SD. (E) Total VEGF levels detected in conditioned media with various co-culture conditions (stromal cells alone +/- healthy donor vs. MF MKs). *p-value <0.05. Data shown represent mean ± SD. (F) Total levels of VEGF in conditioned media (CM) of cultured stromal cells, either alone or together with healthy vs. MF MKs with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD.

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet: (A) Ratio of total CD33+ cell output relative to untreated of cultured healthy donor (HD; light blue) vs. myelofibrosis (MF; dark blue) CD34+ cells in response to exogenous CXCL8 doses (50ng vs. 100ng) with or without the CXCR1/2 inhibitor Ladarixin (10uM). *p<0.05. Data shown represent mean ± SD. (B) Ratio of total CD41+ cell output relative to untreated of cultured healthy donor (HD; light blue) vs. myelofibrosis (MF; dark blue) CD34+ cells in response to exogenous CXCL8 doses (50ng vs. 100ng) with or without the CXCR1/2 inhibitor Ladarixin (10uM). *p<0.05. Data shown represent mean ± SD. (C) Fold-change in detectable VEGF levels in conditioned media (CM) elicited by either healthy donor vs. MF megakaryocytes (MKs) with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD. (D) Total CXCL8 levels detected in conditioned media of various co-culture conditions (stromal cells alone +/- healthy donor or MF megakaryocytes [MK]). *p-value <0.05. Data shown represent mean ± SD. (E) Total VEGF levels detected in conditioned media with various co-culture conditions (stromal cells alone +/- healthy donor vs. MF MKs). *p-value <0.05. Data shown represent mean ± SD. (F) Total levels of VEGF in conditioned media (CM) of cultured stromal cells, either alone or together with healthy vs. MF MKs with or without the addition of reparixin (REP; 10uM). *p-value <0.05. Data shown represent mean ± SD.

Techniques: Cell Culture, Co-Culture Assay

Journal: bioRxiv

Article Title: CXCL8/CXCR2 signaling mediates bone marrow fibrosis and represents a therapeutic target in myelofibrosis

doi: 10.1101/2021.12.08.471791

Figure Lengend Snippet:

Techniques: Inhibition

Review

Structured Review

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1) Product Images from "Scaffolds with spatiotemporally controlled growth factor delivery and cyclodextrin-enabled antagonism of growth factor receptor sequestration promote cutaneous wound healing"

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