dmba  (Worthington Biochemical)


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    Name:
    Collagenase Type 5
    Description:
    Prepared to contain higher collagenase and caseinase activities A dialyzed lyophilized powder
    Catalog Number:
    ls005280
    Price:
    42
    Size:
    100 mg
    Source:
    Clostridium histolyticum
    Cas Number:
    9001.12.1
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    Structured Review

    Worthington Biochemical dmba
    The TG overexpression of VEGF-D affects inflammatory cell accumulation in skin tumors. Representative photographs of CD4 + (A) and CD8 + (C) T-cells and F4/80 + macrophages (E) in the peritumoral area of WT and TG papillomas at week 20. The number of CD4 + (B) and CD8 + T-cells (D), and macrophages (F) in the UT skin, <t>TPA-treated</t> skin, PAPs and cSCCs collected at different time points of skin carcinogenesis. VEGF-D overexpression resulted in significantly less CD4 + T-cells and macrophages, and more CD8 + T-cells in skin tumors at several time points of skin carcinogenesis. (G) FACS analysis revealed significantly less CD4 + T-cells (CD3 + CD4 + Gr-1 − ) and macrophages (Gr-1 − CD11b + F4/80 + ), and significantly more CD8 + T-cells (CD3 + CD8 + Gr-1 − ) in the <t>DMBA-TPA</t> treated skin of the TG mice (N = 5) than in the WT mice (N = 6) at week 10 of carcinogenesis. Scale bars: 100 μm (A, E) and 50 μm (C). Error bars: SD. *: P
    Prepared to contain higher collagenase and caseinase activities A dialyzed lyophilized powder
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    Images

    1) Product Images from "Elevated VEGF-D Modulates Tumor Inflammation and Reduces the Growth of Carcinogen-Induced Skin Tumors"

    Article Title: Elevated VEGF-D Modulates Tumor Inflammation and Reduces the Growth of Carcinogen-Induced Skin Tumors

    Journal: Neoplasia (New York, N.Y.)

    doi: 10.1016/j.neo.2016.05.002

    The TG overexpression of VEGF-D affects inflammatory cell accumulation in skin tumors. Representative photographs of CD4 + (A) and CD8 + (C) T-cells and F4/80 + macrophages (E) in the peritumoral area of WT and TG papillomas at week 20. The number of CD4 + (B) and CD8 + T-cells (D), and macrophages (F) in the UT skin, TPA-treated skin, PAPs and cSCCs collected at different time points of skin carcinogenesis. VEGF-D overexpression resulted in significantly less CD4 + T-cells and macrophages, and more CD8 + T-cells in skin tumors at several time points of skin carcinogenesis. (G) FACS analysis revealed significantly less CD4 + T-cells (CD3 + CD4 + Gr-1 − ) and macrophages (Gr-1 − CD11b + F4/80 + ), and significantly more CD8 + T-cells (CD3 + CD8 + Gr-1 − ) in the DMBA-TPA treated skin of the TG mice (N = 5) than in the WT mice (N = 6) at week 10 of carcinogenesis. Scale bars: 100 μm (A, E) and 50 μm (C). Error bars: SD. *: P
    Figure Legend Snippet: The TG overexpression of VEGF-D affects inflammatory cell accumulation in skin tumors. Representative photographs of CD4 + (A) and CD8 + (C) T-cells and F4/80 + macrophages (E) in the peritumoral area of WT and TG papillomas at week 20. The number of CD4 + (B) and CD8 + T-cells (D), and macrophages (F) in the UT skin, TPA-treated skin, PAPs and cSCCs collected at different time points of skin carcinogenesis. VEGF-D overexpression resulted in significantly less CD4 + T-cells and macrophages, and more CD8 + T-cells in skin tumors at several time points of skin carcinogenesis. (G) FACS analysis revealed significantly less CD4 + T-cells (CD3 + CD4 + Gr-1 − ) and macrophages (Gr-1 − CD11b + F4/80 + ), and significantly more CD8 + T-cells (CD3 + CD8 + Gr-1 − ) in the DMBA-TPA treated skin of the TG mice (N = 5) than in the WT mice (N = 6) at week 10 of carcinogenesis. Scale bars: 100 μm (A, E) and 50 μm (C). Error bars: SD. *: P

    Techniques Used: Over Expression, Papanicolaou Stain, FACS, Mouse Assay

    DMBA-TPA-induced skin carcinogenesis in VEGF-D knockout mice. Tumor incidence (A) and cumulative multiplicity (B) in the KO males (N = 26) and the WT males (N = 27) did not show statistically significant differences between the genotypes. ( C-D ) Expression of VEGF-D in mouse skin tumors. Representative immunohistochemical stainings showing VEGF-D expression in mouse cSCCs. (C) Consecutive sections of the WT cSCC stained with antibodies against VEGF-D and F4/80 demonstrate that VEGF-D is expressed by F4/80-positive macrophages (arrowheads) within the WT cSCC stroma. Asterisks indicate vessels that facilitate the identification of co-stained cells in the consecutive sections. (D) VEGF-D expression by invasive carcinoma cells (arrowheads) within the WT cSCC. The KO cSCC is used as a negative control for VEGF-D staining. (E) The quantification of lymphatic vessel density in the untreated (UT) skin, TPA-treated skin, and papillomas (PAP) and cSCCs collected at different time points of skin carcinogenesis. The KO tumors showed a trend for reduced lymphangiogenesis. In the UT skin, and in cSCCs at week 29, the difference between the genotypes was significant. (F) No significant differences in blood vessel densities between the KO and WT males in any type of sample. Scale bars: 50 μm (C) and 100 μm (D): Error bars: SD. *: P
    Figure Legend Snippet: DMBA-TPA-induced skin carcinogenesis in VEGF-D knockout mice. Tumor incidence (A) and cumulative multiplicity (B) in the KO males (N = 26) and the WT males (N = 27) did not show statistically significant differences between the genotypes. ( C-D ) Expression of VEGF-D in mouse skin tumors. Representative immunohistochemical stainings showing VEGF-D expression in mouse cSCCs. (C) Consecutive sections of the WT cSCC stained with antibodies against VEGF-D and F4/80 demonstrate that VEGF-D is expressed by F4/80-positive macrophages (arrowheads) within the WT cSCC stroma. Asterisks indicate vessels that facilitate the identification of co-stained cells in the consecutive sections. (D) VEGF-D expression by invasive carcinoma cells (arrowheads) within the WT cSCC. The KO cSCC is used as a negative control for VEGF-D staining. (E) The quantification of lymphatic vessel density in the untreated (UT) skin, TPA-treated skin, and papillomas (PAP) and cSCCs collected at different time points of skin carcinogenesis. The KO tumors showed a trend for reduced lymphangiogenesis. In the UT skin, and in cSCCs at week 29, the difference between the genotypes was significant. (F) No significant differences in blood vessel densities between the KO and WT males in any type of sample. Scale bars: 50 μm (C) and 100 μm (D): Error bars: SD. *: P

    Techniques Used: Knock-Out, Mouse Assay, Expressing, Immunohistochemistry, Staining, Negative Control

    Impaired skin tumor formation in TG K14-mVEGF-D mice in a chemical skin carcinogenesis model. Tumors were induced in the mouse skin using a multistage DMBA-TPA protocol and their growth was monitored for up to 30 weeks (Wk). Data from two separate experimental groups of males (WT N = 23, TG N = 25) are combined. (A) Representative photographs of the WT and K14-mVEGF-D TG male mice at different time points. Black arrowheads indicate exophytic papillomas and white arrowheads regressing papillomas. (B) Tumor incidence showed a significant delay in the TG mice. (C) The TG mice developed markedly less tumors than the WT mice. Cumulative tumor multiplicity is shown. (D) The percentage of regressing papillomas (the black portion of the column) was higher in the TG mice (red) than in the WT mice (green). (E) Smaller tumor size in the TG mice than in the WT mice. Tumor sizes are shown as a percentage of tumors in three different size categories. Statistical significance for each size category is shown in between the column pairs. (F) At weeks 20–30 the percentage of TG male mice with clinically apparent cSCC was lower than that of WT control males. (G) A trend towards less cSCCs per mouse was observed in TG males. N = number of mice. Error bars: SD.*: P
    Figure Legend Snippet: Impaired skin tumor formation in TG K14-mVEGF-D mice in a chemical skin carcinogenesis model. Tumors were induced in the mouse skin using a multistage DMBA-TPA protocol and their growth was monitored for up to 30 weeks (Wk). Data from two separate experimental groups of males (WT N = 23, TG N = 25) are combined. (A) Representative photographs of the WT and K14-mVEGF-D TG male mice at different time points. Black arrowheads indicate exophytic papillomas and white arrowheads regressing papillomas. (B) Tumor incidence showed a significant delay in the TG mice. (C) The TG mice developed markedly less tumors than the WT mice. Cumulative tumor multiplicity is shown. (D) The percentage of regressing papillomas (the black portion of the column) was higher in the TG mice (red) than in the WT mice (green). (E) Smaller tumor size in the TG mice than in the WT mice. Tumor sizes are shown as a percentage of tumors in three different size categories. Statistical significance for each size category is shown in between the column pairs. (F) At weeks 20–30 the percentage of TG male mice with clinically apparent cSCC was lower than that of WT control males. (G) A trend towards less cSCCs per mouse was observed in TG males. N = number of mice. Error bars: SD.*: P

    Techniques Used: Mouse Assay

    2) Product Images from "Antioxidant Peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo"

    Article Title: Antioxidant Peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo

    Journal: Neurochemistry international

    doi: 10.1016/j.neuint.2015.08.006

    Prdx6 expression in nonTg, Prdx6 Tg and Prdx6 KO animals. ( A ) Western blot analysis to confirm Prdx6 expression. Primary neurons, primary astrocytes and brain homogenates from naïve wild type nonTg, Prdx6 Tg and Prdx6 KO animals were probed for
    Figure Legend Snippet: Prdx6 expression in nonTg, Prdx6 Tg and Prdx6 KO animals. ( A ) Western blot analysis to confirm Prdx6 expression. Primary neurons, primary astrocytes and brain homogenates from naïve wild type nonTg, Prdx6 Tg and Prdx6 KO animals were probed for

    Techniques Used: Expressing, Western Blot

    ( A ) MTT assay showing that TAT-Prdx6 (5ug/ml) attenuates H 2 O 2 and CoCl 2 mediated cytotoxicity in SK-N-SH human neuroblastoma cells. Cells were cultured and treated for 48 h with indicated concentrations of H 2 O 2 and CoCl 2 . The capacity of the cells to
    Figure Legend Snippet: ( A ) MTT assay showing that TAT-Prdx6 (5ug/ml) attenuates H 2 O 2 and CoCl 2 mediated cytotoxicity in SK-N-SH human neuroblastoma cells. Cells were cultured and treated for 48 h with indicated concentrations of H 2 O 2 and CoCl 2 . The capacity of the cells to

    Techniques Used: MTT Assay, Cell Culture

    Representative western blots showing change in prion related biochemistry representative of n=6 per group. We observed a significant increase in PrP immunoreactivity (IR) (PrP C /PrP Sc ) as detected by anti-PrP 6D11 mAb in nonTg, Prdx6 KO and Prdx6 Tg-ME7
    Figure Legend Snippet: Representative western blots showing change in prion related biochemistry representative of n=6 per group. We observed a significant increase in PrP immunoreactivity (IR) (PrP C /PrP Sc ) as detected by anti-PrP 6D11 mAb in nonTg, Prdx6 KO and Prdx6 Tg-ME7

    Techniques Used: Western Blot

    3) Product Images from "Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis"

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.09.018

    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
    Figure Legend Snippet: TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Techniques Used: Mouse Assay, In Vivo, Labeling, Blocking Assay, Injection, Transmission Electron Microscopy

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.
    Figure Legend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Techniques Used: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    4) Product Images from "Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis"

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.09.018

    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
    Figure Legend Snippet: TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Techniques Used: Mouse Assay, In Vivo, Labeling, Blocking Assay, Injection, Transmission Electron Microscopy

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.
    Figure Legend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Techniques Used: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    5) Product Images from "Multipotent luminal mammary cancer stem cells model tumor heterogeneity"

    Article Title: Multipotent luminal mammary cancer stem cells model tumor heterogeneity

    Journal: Breast Cancer Research : BCR

    doi: 10.1186/s13058-015-0615-y

    MaCSCs have the capacity to differentiate into multiple cell types. ( a ) A single Py230 cell stained with myoepithelial marker keratin 14 (K14) and luminal marker keratin 8 (K8). ( b ) Clonal Py230 cells grown on a glass coverslip stained with K14 and K8. Scale bar 20 μm. ( c ) Clonogenic efficiency of C57Bl/6 MaCSC line Py230 and FVB/N MaCSC line Py9813. ( d ) Hollow mammospheres of Py230 cells in suspension culture. Scale bar 50 μm. ( e,f ) Py230 mammosphere stained with K14 and K8. Scale bar 20 μm. ( g ) Py230 mammosphere grown on collagen exhibits branching structures. Scale bar 100 μm. ( h ) Confluent Py230 cells spontaneously form domes. ( i ) Domes become enlarged upon treatment with lactogenic hormones dexamethasone and prolactin. Scale bar 50 μm. ( j ) Expression of beta-casein by MaCSC lines Py230 and Py9813 following treatment with lactogenic hormones. Data are means ± SEM of triplicate samples. ( k ) Py230 cells treated with retinoic acid and rosiglitazone express genes associated with adipocyte differentiation. Data are means ± SEM of triplicate samples. Inset: Py230 cells stained with oil red O. Scale bar 10 μm
    Figure Legend Snippet: MaCSCs have the capacity to differentiate into multiple cell types. ( a ) A single Py230 cell stained with myoepithelial marker keratin 14 (K14) and luminal marker keratin 8 (K8). ( b ) Clonal Py230 cells grown on a glass coverslip stained with K14 and K8. Scale bar 20 μm. ( c ) Clonogenic efficiency of C57Bl/6 MaCSC line Py230 and FVB/N MaCSC line Py9813. ( d ) Hollow mammospheres of Py230 cells in suspension culture. Scale bar 50 μm. ( e,f ) Py230 mammosphere stained with K14 and K8. Scale bar 20 μm. ( g ) Py230 mammosphere grown on collagen exhibits branching structures. Scale bar 100 μm. ( h ) Confluent Py230 cells spontaneously form domes. ( i ) Domes become enlarged upon treatment with lactogenic hormones dexamethasone and prolactin. Scale bar 50 μm. ( j ) Expression of beta-casein by MaCSC lines Py230 and Py9813 following treatment with lactogenic hormones. Data are means ± SEM of triplicate samples. ( k ) Py230 cells treated with retinoic acid and rosiglitazone express genes associated with adipocyte differentiation. Data are means ± SEM of triplicate samples. Inset: Py230 cells stained with oil red O. Scale bar 10 μm

    Techniques Used: Staining, Marker, Expressing

    6) Product Images from "Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis"

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    Journal: Immunity

    doi: 10.1016/j.immuni.2018.09.018

    CXCL1 and CXCL2 Are Differentially Expressed in TNF-Stimulated Tissues (A–E) WT mice were treated i.s. with PBS or TNF and cremaster muscles were IF stained for CXCL1 or CXCL2 and CD31 (ECs), α-SMA (pericytes), and MRP14 (neutrophils). Representative confocal images of venules showing CXCL1 (A) or CXCL2 (C) staining within EC and pericyte isosurface masks and quantifications of CXCL1 (B) and CXCL2 (D) in ECs or pericytes, in terms of MFIs (n = 4 mice per group) from 4 independent experiments. (E) Confocal abluminal and cross-sectional images (acquired along the dashed line and presented at 90° rotation) of a venule showing overall CXCL2 staining representative of 4 independent experiments. (F) Cxcl1 and Cxcl2 mRNA levels relative to Gapdh in circulating neutrophils 2–3 hr after i.s. PBS or TNF injection as determined by real-time PCR (n = 4–5 mice per group, 2 independent experiments). (G–J) Purified mouse bone marrow neutrophils were treated with PBS or TNF (1 nM, 1 hr) on uncoated (G, H), BSA-coated, or CXCL1-coated wells (I, J). CXCL1 and/or CXCL2 levels in lysates (G and I) and supernatants (H and J) as quantified by ELISA (n = 4–12) from 2–4 independent experiments. Means ± SEM, ∗ p
    Figure Legend Snippet: CXCL1 and CXCL2 Are Differentially Expressed in TNF-Stimulated Tissues (A–E) WT mice were treated i.s. with PBS or TNF and cremaster muscles were IF stained for CXCL1 or CXCL2 and CD31 (ECs), α-SMA (pericytes), and MRP14 (neutrophils). Representative confocal images of venules showing CXCL1 (A) or CXCL2 (C) staining within EC and pericyte isosurface masks and quantifications of CXCL1 (B) and CXCL2 (D) in ECs or pericytes, in terms of MFIs (n = 4 mice per group) from 4 independent experiments. (E) Confocal abluminal and cross-sectional images (acquired along the dashed line and presented at 90° rotation) of a venule showing overall CXCL2 staining representative of 4 independent experiments. (F) Cxcl1 and Cxcl2 mRNA levels relative to Gapdh in circulating neutrophils 2–3 hr after i.s. PBS or TNF injection as determined by real-time PCR (n = 4–5 mice per group, 2 independent experiments). (G–J) Purified mouse bone marrow neutrophils were treated with PBS or TNF (1 nM, 1 hr) on uncoated (G, H), BSA-coated, or CXCL1-coated wells (I, J). CXCL1 and/or CXCL2 levels in lysates (G and I) and supernatants (H and J) as quantified by ELISA (n = 4–12) from 2–4 independent experiments. Means ± SEM, ∗ p

    Techniques Used: Mouse Assay, Staining, Injection, Real-time Polymerase Chain Reaction, Purification, Enzyme-linked Immunosorbent Assay

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.
    Figure Legend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Techniques Used: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    TNF-Induced Neutrophil Migration Is Dependent on Both CXCL1 and CXCL2 WT mice pre-treated intrascrotally (i.s.) with control (ctr) or blocking mAbs or Cxcr2 −/− mice were subjected to i.s. injections of PBS or TNF. The cremaster muscles were immunostained for MRP14 (neutrophils) and α-SMA (pericytes) and analyzed for neutrophil infiltration by confocal microscopy. (A) and (C) are representative images and (B), (D), and (E) show quantifications (n = 4–10 mice per group) from 5–6 independent experiments. Means ± SEM, ∗∗∗ p
    Figure Legend Snippet: TNF-Induced Neutrophil Migration Is Dependent on Both CXCL1 and CXCL2 WT mice pre-treated intrascrotally (i.s.) with control (ctr) or blocking mAbs or Cxcr2 −/− mice were subjected to i.s. injections of PBS or TNF. The cremaster muscles were immunostained for MRP14 (neutrophils) and α-SMA (pericytes) and analyzed for neutrophil infiltration by confocal microscopy. (A) and (C) are representative images and (B), (D), and (E) show quantifications (n = 4–10 mice per group) from 5–6 independent experiments. Means ± SEM, ∗∗∗ p

    Techniques Used: Migration, Mouse Assay, Blocking Assay, Confocal Microscopy

    7) Product Images from "Multipotent luminal mammary cancer stem cells model tumor heterogeneity"

    Article Title: Multipotent luminal mammary cancer stem cells model tumor heterogeneity

    Journal: Breast Cancer Research : BCR

    doi: 10.1186/s13058-015-0615-y

    Py230 mammary cancer stem cells recapitulate spontaneous luminal tumorigenesis and metastasis. a-f , H E stained sections of Py230 MIN ( a ), tumor ( b ) and metastasis ( c ) compared with spontaneous PyVmT MIN, ( d ), tumor ( e ) and metastasis ( f ). Scale bar = 50 μm. g-j Whole mounts of normal mammary gland (NMG), pre-lactating mammary gland (PLMG), PyVmT MIN and a 10-day outgrowth of Py230 tumor cells in the cleared mammary fat pad. Scale bar = 100 μm. k-r , Representative dot plots of NMG ( k,o ), PLMG ( l,p ), PyVmT MIN ( m,q ) and Py230 tumor ( n,r ) labeled with CD24 and CD49f ( k-n ) or CD24 and CD29 ( o-r )
    Figure Legend Snippet: Py230 mammary cancer stem cells recapitulate spontaneous luminal tumorigenesis and metastasis. a-f , H E stained sections of Py230 MIN ( a ), tumor ( b ) and metastasis ( c ) compared with spontaneous PyVmT MIN, ( d ), tumor ( e ) and metastasis ( f ). Scale bar = 50 μm. g-j Whole mounts of normal mammary gland (NMG), pre-lactating mammary gland (PLMG), PyVmT MIN and a 10-day outgrowth of Py230 tumor cells in the cleared mammary fat pad. Scale bar = 100 μm. k-r , Representative dot plots of NMG ( k,o ), PLMG ( l,p ), PyVmT MIN ( m,q ) and Py230 tumor ( n,r ) labeled with CD24 and CD49f ( k-n ) or CD24 and CD29 ( o-r )

    Techniques Used: Staining, Labeling

    8) Product Images from "Phosphoinositide 3-kinase Akt signaling pathway interacts with protein kinase Cβ2 in the regulation of physiologic developmental hypertrophy and heart function"

    Article Title: Phosphoinositide 3-kinase Akt signaling pathway interacts with protein kinase Cβ2 in the regulation of physiologic developmental hypertrophy and heart function

    Journal:

    doi: 10.1152/ajpheart.00562.2008

    Comparison of organ weights and cardiomyocyte size in transgenic (Tg) mice. A : representation of heart size from wild-type (WT), protein kinase C (PKC) β2, dominant-negative (dn) phosphatidylinositol 3-kinase [PI3-kinase (PI3K)],
    Figure Legend Snippet: Comparison of organ weights and cardiomyocyte size in transgenic (Tg) mice. A : representation of heart size from wild-type (WT), protein kinase C (PKC) β2, dominant-negative (dn) phosphatidylinositol 3-kinase [PI3-kinase (PI3K)],

    Techniques Used: Transgenic Assay, Mouse Assay, Dominant Negative Mutation

    9) Product Images from "Elevated VEGF-D Modulates Tumor Inflammation and Reduces the Growth of Carcinogen-Induced Skin Tumors 1"

    Article Title: Elevated VEGF-D Modulates Tumor Inflammation and Reduces the Growth of Carcinogen-Induced Skin Tumors 1

    Journal: Neoplasia (New York, N.Y.)

    doi: 10.1016/j.neo.2016.05.002

    The TG overexpression of VEGF-D affects inflammatory cell accumulation in skin tumors. Representative photographs of CD4 + (A) and CD8 + (C) T-cells and F4/80 + macrophages (E) in the peritumoral area of WT and TG papillomas at week 20. The number of CD4 + (B) and CD8 + T-cells (D), and macrophages (F) in the UT skin, TPA-treated skin, PAPs and cSCCs collected at different time points of skin carcinogenesis. VEGF-D overexpression resulted in significantly less CD4 + T-cells and macrophages, and more CD8 + T-cells in skin tumors at several time points of skin carcinogenesis. (G) FACS analysis revealed significantly less CD4 + T-cells (CD3 + CD4 + Gr-1 − ) and macrophages (Gr-1 − CD11b + F4/80 + ), and significantly more CD8 + T-cells (CD3 + CD8 + Gr-1 − ) in the DMBA-TPA treated skin of the TG mice (N = 5) than in the WT mice (N = 6) at week 10 of carcinogenesis. Scale bars: 100 μm (A, E) and 50 μm (C). Error bars: SD. *: P
    Figure Legend Snippet: The TG overexpression of VEGF-D affects inflammatory cell accumulation in skin tumors. Representative photographs of CD4 + (A) and CD8 + (C) T-cells and F4/80 + macrophages (E) in the peritumoral area of WT and TG papillomas at week 20. The number of CD4 + (B) and CD8 + T-cells (D), and macrophages (F) in the UT skin, TPA-treated skin, PAPs and cSCCs collected at different time points of skin carcinogenesis. VEGF-D overexpression resulted in significantly less CD4 + T-cells and macrophages, and more CD8 + T-cells in skin tumors at several time points of skin carcinogenesis. (G) FACS analysis revealed significantly less CD4 + T-cells (CD3 + CD4 + Gr-1 − ) and macrophages (Gr-1 − CD11b + F4/80 + ), and significantly more CD8 + T-cells (CD3 + CD8 + Gr-1 − ) in the DMBA-TPA treated skin of the TG mice (N = 5) than in the WT mice (N = 6) at week 10 of carcinogenesis. Scale bars: 100 μm (A, E) and 50 μm (C). Error bars: SD. *: P

    Techniques Used: Over Expression, Papanicolaou Stain, FACS, Mouse Assay

    DMBA-TPA-induced skin carcinogenesis in VEGF-D knockout mice. Tumor incidence (A) and cumulative multiplicity (B) in the KO males (N = 26) and the WT males (N = 27) did not show statistically significant differences between the genotypes. ( C-D ) Expression of VEGF-D in mouse skin tumors. Representative immunohistochemical stainings showing VEGF-D expression in mouse cSCCs. (C) Consecutive sections of the WT cSCC stained with antibodies against VEGF-D and F4/80 demonstrate that VEGF-D is expressed by F4/80-positive macrophages (arrowheads) within the WT cSCC stroma. Asterisks indicate vessels that facilitate the identification of co-stained cells in the consecutive sections. (D) VEGF-D expression by invasive carcinoma cells (arrowheads) within the WT cSCC. The KO cSCC is used as a negative control for VEGF-D staining. (E) The quantification of lymphatic vessel density in the untreated (UT) skin, TPA-treated skin, and papillomas (PAP) and cSCCs collected at different time points of skin carcinogenesis. The KO tumors showed a trend for reduced lymphangiogenesis. In the UT skin, and in cSCCs at week 29, the difference between the genotypes was significant. (F) No significant differences in blood vessel densities between the KO and WT males in any type of sample. Scale bars: 50 μm (C) and 100 μm (D): Error bars: SD. *: P
    Figure Legend Snippet: DMBA-TPA-induced skin carcinogenesis in VEGF-D knockout mice. Tumor incidence (A) and cumulative multiplicity (B) in the KO males (N = 26) and the WT males (N = 27) did not show statistically significant differences between the genotypes. ( C-D ) Expression of VEGF-D in mouse skin tumors. Representative immunohistochemical stainings showing VEGF-D expression in mouse cSCCs. (C) Consecutive sections of the WT cSCC stained with antibodies against VEGF-D and F4/80 demonstrate that VEGF-D is expressed by F4/80-positive macrophages (arrowheads) within the WT cSCC stroma. Asterisks indicate vessels that facilitate the identification of co-stained cells in the consecutive sections. (D) VEGF-D expression by invasive carcinoma cells (arrowheads) within the WT cSCC. The KO cSCC is used as a negative control for VEGF-D staining. (E) The quantification of lymphatic vessel density in the untreated (UT) skin, TPA-treated skin, and papillomas (PAP) and cSCCs collected at different time points of skin carcinogenesis. The KO tumors showed a trend for reduced lymphangiogenesis. In the UT skin, and in cSCCs at week 29, the difference between the genotypes was significant. (F) No significant differences in blood vessel densities between the KO and WT males in any type of sample. Scale bars: 50 μm (C) and 100 μm (D): Error bars: SD. *: P

    Techniques Used: Knock-Out, Mouse Assay, Expressing, Immunohistochemistry, Staining, Negative Control

    Impaired skin tumor formation in TG K14-mVEGF-D mice in a chemical skin carcinogenesis model. Tumors were induced in the mouse skin using a multistage DMBA-TPA protocol and their growth was monitored for up to 30 weeks (Wk). Data from two separate experimental groups of males (WT N = 23, TG N = 25) are combined. (A) Representative photographs of the WT and K14-mVEGF-D TG male mice at different time points. Black arrowheads indicate exophytic papillomas and white arrowheads regressing papillomas. (B) Tumor incidence showed a significant delay in the TG mice. (C) The TG mice developed markedly less tumors than the WT mice. Cumulative tumor multiplicity is shown. (D) The percentage of regressing papillomas (the black portion of the column) was higher in the TG mice (red) than in the WT mice (green). (E) Smaller tumor size in the TG mice than in the WT mice. Tumor sizes are shown as a percentage of tumors in three different size categories. Statistical significance for each size category is shown in between the column pairs. (F) At weeks 20–30 the percentage of TG male mice with clinically apparent cSCC was lower than that of WT control males. (G) A trend towards less cSCCs per mouse was observed in TG males. N = number of mice. Error bars: SD.*: P
    Figure Legend Snippet: Impaired skin tumor formation in TG K14-mVEGF-D mice in a chemical skin carcinogenesis model. Tumors were induced in the mouse skin using a multistage DMBA-TPA protocol and their growth was monitored for up to 30 weeks (Wk). Data from two separate experimental groups of males (WT N = 23, TG N = 25) are combined. (A) Representative photographs of the WT and K14-mVEGF-D TG male mice at different time points. Black arrowheads indicate exophytic papillomas and white arrowheads regressing papillomas. (B) Tumor incidence showed a significant delay in the TG mice. (C) The TG mice developed markedly less tumors than the WT mice. Cumulative tumor multiplicity is shown. (D) The percentage of regressing papillomas (the black portion of the column) was higher in the TG mice (red) than in the WT mice (green). (E) Smaller tumor size in the TG mice than in the WT mice. Tumor sizes are shown as a percentage of tumors in three different size categories. Statistical significance for each size category is shown in between the column pairs. (F) At weeks 20–30 the percentage of TG male mice with clinically apparent cSCC was lower than that of WT control males. (G) A trend towards less cSCCs per mouse was observed in TG males. N = number of mice. Error bars: SD.*: P

    Techniques Used: Mouse Assay

    10) Product Images from "A CK1α Activator Penetrates the Brain and Shows Efficacy Against Drug-resistant Metastatic Medulloblastoma"

    Article Title: A CK1α Activator Penetrates the Brain and Shows Efficacy Against Drug-resistant Metastatic Medulloblastoma

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    doi: 10.1158/1078-0432.CCR-18-1319

    SSTC3 acts downstream of SMO to attenuate SHH activity. A, LIGHT2 cells were treated with 1 μg/mL recombinant SHH for 24 hours, followed by addition of the indicated concentrations of SSTC3 or SSTC111 for an additional 48 hours. Firefly luciferase activity was then determined and normalized to Renilla luciferase activity. B, NIH-3T3 cells were incubated with the SAG (100 nmol/L) and the indicated concentrations of SSTC3. The expression of GLI1 was determined at the indicated timepoints and normalized to that of the housekeeping gene GAPDH . Data were normalized to a vehicle control. C, LIGHT2 cells were transduced with lentivirus expressing the indicated shRNA to generate stable polyclonal cell lines. These cells were treated with SAG (100 nmol/L) and SSTC3 (200 nmol/L) for 48 hours. The expression of GLI1 was determined and normalized to that of GAPDH . D, GPCs were incubated in the presence of DMSO, SAG (100 nmol/L), or SAG (100 nmol/L) and SSTC3 (200 nmol/L), for 24 hours prior to quantification of BrdU incorporation. E, Representative images from similarly treated GPC are shown. F, GPC were treated with vehicle, vismodegib (100 nmol/L), or SAG (100 nmol/L) and SSTC3 (200 nmol/L), and expression of the indicated genes determined 6 hours later. Data were normalized to a SAG-treated vehicle control. G, SUFU −/− MEFs were treated for 48 hours with vehicle, the indicated concentrations of SSTC3, or vismodegib (200 nmol/L). The expression of GLI1 was then determined and normalized to that of GAPDH . Data were normalized to a vehicle control. H, LIGHT2 cells expressing WT SMO , the vismodegib-resistant oncogenic SMO mutant M2-D473 , or GLI1 , were treated with vehicle, vismodegib (200 nmol/L), or SSTC3 (200 nmol/L). Firefly luciferase activity was then determined and normalized to Renilla luciferase activity. Data were normalized to a SMO WT vehicle control. I, The indicated MEFs were treated with SAG (100 nmol/L) and SSTC3 (200 nmol/L) for 24 hours, and the levels of PTCH1 expression determined and normalized to that of housekeeping gene GAPDH by qRT-PCR. Data were normalized to a SAG-treated vehicle control. J, The indicated MEFs were treated with SAG (100 nmol/L) and SSTC3 (200 nmol/L) for 24 hours, and the levels of GLI1 expression determined and normalized to that of housekeeping gene GAPDH by qRT-PCR. Data were normalized to a SAG-treated vehicle control.
    Figure Legend Snippet: SSTC3 acts downstream of SMO to attenuate SHH activity. A, LIGHT2 cells were treated with 1 μg/mL recombinant SHH for 24 hours, followed by addition of the indicated concentrations of SSTC3 or SSTC111 for an additional 48 hours. Firefly luciferase activity was then determined and normalized to Renilla luciferase activity. B, NIH-3T3 cells were incubated with the SAG (100 nmol/L) and the indicated concentrations of SSTC3. The expression of GLI1 was determined at the indicated timepoints and normalized to that of the housekeeping gene GAPDH . Data were normalized to a vehicle control. C, LIGHT2 cells were transduced with lentivirus expressing the indicated shRNA to generate stable polyclonal cell lines. These cells were treated with SAG (100 nmol/L) and SSTC3 (200 nmol/L) for 48 hours. The expression of GLI1 was determined and normalized to that of GAPDH . D, GPCs were incubated in the presence of DMSO, SAG (100 nmol/L), or SAG (100 nmol/L) and SSTC3 (200 nmol/L), for 24 hours prior to quantification of BrdU incorporation. E, Representative images from similarly treated GPC are shown. F, GPC were treated with vehicle, vismodegib (100 nmol/L), or SAG (100 nmol/L) and SSTC3 (200 nmol/L), and expression of the indicated genes determined 6 hours later. Data were normalized to a SAG-treated vehicle control. G, SUFU −/− MEFs were treated for 48 hours with vehicle, the indicated concentrations of SSTC3, or vismodegib (200 nmol/L). The expression of GLI1 was then determined and normalized to that of GAPDH . Data were normalized to a vehicle control. H, LIGHT2 cells expressing WT SMO , the vismodegib-resistant oncogenic SMO mutant M2-D473 , or GLI1 , were treated with vehicle, vismodegib (200 nmol/L), or SSTC3 (200 nmol/L). Firefly luciferase activity was then determined and normalized to Renilla luciferase activity. Data were normalized to a SMO WT vehicle control. I, The indicated MEFs were treated with SAG (100 nmol/L) and SSTC3 (200 nmol/L) for 24 hours, and the levels of PTCH1 expression determined and normalized to that of housekeeping gene GAPDH by qRT-PCR. Data were normalized to a SAG-treated vehicle control. J, The indicated MEFs were treated with SAG (100 nmol/L) and SSTC3 (200 nmol/L) for 24 hours, and the levels of GLI1 expression determined and normalized to that of housekeeping gene GAPDH by qRT-PCR. Data were normalized to a SAG-treated vehicle control.

    Techniques Used: Activity Assay, Recombinant, Luciferase, Incubation, Expressing, Transduction, shRNA, BrdU Incorporation Assay, Gel Permeation Chromatography, Mutagenesis, Quantitative RT-PCR

    SSTC3 increases the symptom-free survival of a GEMM of SHH subgroup medulloblastoma. A, SAG (100 nmol/L)-induced WT- or ND2:SMOA1 -derived GPC were treated with the indicated concentrations of vismodegib or SSTC3. GPC proliferation was subsequently determined by BrdU incorporation 24 hours later. Data were normalized to a vehicle control. B, Two-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (20 mg/kg i.p. in DMSO) daily for 1 month. Representative IVIS images from vehicle or SSTC3-treated mice are shown. C, Similar mice were treated every other day with SSTC3 (10 mg/kg i.p. in DMSO) for a month. Representative images of brains and H E staining from WT vehicle, ND2:SMOA1 vehicle, or SSTC3-treated mice are shown. D, The area of tumor from the vehicle and SSTC3-treated mice was determined ( N = 6). E, Metastatic lesions were quantified from similarly treated mice ( N = 6). F, Tumors from these mice were immunostained for the proliferation biomarker PCNA and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. G, Representative images of PCNA immunostaining are shown. H, Orthotopic tumors were immunostained for the apoptosis biomarker Cleaved CASPASE-3 and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. I, Representative images of Cleaved CASPASE-3 immunostaining are shown. J, Four-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (10 mg/kg i.p. in DMSO) for 2 consecutive days. The mice were then sacrificed and their cerebella harvested 6 hours after the last injection. The expression of the indicated genes was then determined and normalized to the expression of GAPDH . Data was normalized to a vehicle control ( N = 5). K, The levels of indicated proteins in similarly treated mice were determined by immunoblotting from a cohort of vehicle (1–5) or SSTC3 (6–10)-treated mice. L, Two-month-old ND2:SMOA1 mice were treated with SSTC3 (10 mg/kg i.p. in DMSO) every other day for 1 month and medulloblastoma symptom-free survival monitored for 9 additional months ( N = 10).
    Figure Legend Snippet: SSTC3 increases the symptom-free survival of a GEMM of SHH subgroup medulloblastoma. A, SAG (100 nmol/L)-induced WT- or ND2:SMOA1 -derived GPC were treated with the indicated concentrations of vismodegib or SSTC3. GPC proliferation was subsequently determined by BrdU incorporation 24 hours later. Data were normalized to a vehicle control. B, Two-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (20 mg/kg i.p. in DMSO) daily for 1 month. Representative IVIS images from vehicle or SSTC3-treated mice are shown. C, Similar mice were treated every other day with SSTC3 (10 mg/kg i.p. in DMSO) for a month. Representative images of brains and H E staining from WT vehicle, ND2:SMOA1 vehicle, or SSTC3-treated mice are shown. D, The area of tumor from the vehicle and SSTC3-treated mice was determined ( N = 6). E, Metastatic lesions were quantified from similarly treated mice ( N = 6). F, Tumors from these mice were immunostained for the proliferation biomarker PCNA and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. G, Representative images of PCNA immunostaining are shown. H, Orthotopic tumors were immunostained for the apoptosis biomarker Cleaved CASPASE-3 and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. I, Representative images of Cleaved CASPASE-3 immunostaining are shown. J, Four-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (10 mg/kg i.p. in DMSO) for 2 consecutive days. The mice were then sacrificed and their cerebella harvested 6 hours after the last injection. The expression of the indicated genes was then determined and normalized to the expression of GAPDH . Data was normalized to a vehicle control ( N = 5). K, The levels of indicated proteins in similarly treated mice were determined by immunoblotting from a cohort of vehicle (1–5) or SSTC3 (6–10)-treated mice. L, Two-month-old ND2:SMOA1 mice were treated with SSTC3 (10 mg/kg i.p. in DMSO) every other day for 1 month and medulloblastoma symptom-free survival monitored for 9 additional months ( N = 10).

    Techniques Used: Derivative Assay, Gel Permeation Chromatography, BrdU Incorporation Assay, Mouse Assay, Staining, Biomarker Assay, Immunostaining, Injection, Expressing

    11) Product Images from "A CK1α Activator Penetrates the Brain and Shows Efficacy Against Drug-resistant Metastatic Medulloblastoma"

    Article Title: A CK1α Activator Penetrates the Brain and Shows Efficacy Against Drug-resistant Metastatic Medulloblastoma

    Journal: Clinical cancer research : an official journal of the American Association for Cancer Research

    doi: 10.1158/1078-0432.CCR-18-1319

    SSTC3 increases the symptom-free survival of a GEMM of SHH subgroup medulloblastoma. A, SAG (100 nmol/L)-induced WT- or ND2:SMOA1 -derived GPC were treated with the indicated concentrations of vismodegib or SSTC3. GPC proliferation was subsequently determined by BrdU incorporation 24 hours later. Data were normalized to a vehicle control. B, Two-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (20 mg/kg i.p. in DMSO) daily for 1 month. Representative IVIS images from vehicle or SSTC3-treated mice are shown. C, Similar mice were treated every other day with SSTC3 (10 mg/kg i.p. in DMSO) for a month. Representative images of brains and H E staining from WT vehicle, ND2:SMOA1 vehicle, or SSTC3-treated mice are shown. D, The area of tumor from the vehicle and SSTC3-treated mice was determined ( N = 6). E, Metastatic lesions were quantified from similarly treated mice ( N = 6). F, Tumors from these mice were immunostained for the proliferation biomarker PCNA and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. G, Representative images of PCNA immunostaining are shown. H, Orthotopic tumors were immunostained for the apoptosis biomarker Cleaved CASPASE-3 and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. I, Representative images of Cleaved CASPASE-3 immunostaining are shown. J, Four-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (10 mg/kg i.p. in DMSO) for 2 consecutive days. The mice were then sacrificed and their cerebella harvested 6 hours after the last injection. The expression of the indicated genes was then determined and normalized to the expression of GAPDH . Data was normalized to a vehicle control ( N = 5). K, The levels of indicated proteins in similarly treated mice were determined by immunoblotting from a cohort of vehicle (1–5) or SSTC3 (6–10)-treated mice. L, Two-month-old ND2:SMOA1 mice were treated with SSTC3 (10 mg/kg i.p. in DMSO) every other day for 1 month and medulloblastoma symptom-free survival monitored for 9 additional months ( N = 10).
    Figure Legend Snippet: SSTC3 increases the symptom-free survival of a GEMM of SHH subgroup medulloblastoma. A, SAG (100 nmol/L)-induced WT- or ND2:SMOA1 -derived GPC were treated with the indicated concentrations of vismodegib or SSTC3. GPC proliferation was subsequently determined by BrdU incorporation 24 hours later. Data were normalized to a vehicle control. B, Two-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (20 mg/kg i.p. in DMSO) daily for 1 month. Representative IVIS images from vehicle or SSTC3-treated mice are shown. C, Similar mice were treated every other day with SSTC3 (10 mg/kg i.p. in DMSO) for a month. Representative images of brains and H E staining from WT vehicle, ND2:SMOA1 vehicle, or SSTC3-treated mice are shown. D, The area of tumor from the vehicle and SSTC3-treated mice was determined ( N = 6). E, Metastatic lesions were quantified from similarly treated mice ( N = 6). F, Tumors from these mice were immunostained for the proliferation biomarker PCNA and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. G, Representative images of PCNA immunostaining are shown. H, Orthotopic tumors were immunostained for the apoptosis biomarker Cleaved CASPASE-3 and the numbers of positive cells per field in 4 fields from 3 independent mice quantified. I, Representative images of Cleaved CASPASE-3 immunostaining are shown. J, Four-month-old ND2:SMOA1 mice were treated with vehicle or SSTC3 (10 mg/kg i.p. in DMSO) for 2 consecutive days. The mice were then sacrificed and their cerebella harvested 6 hours after the last injection. The expression of the indicated genes was then determined and normalized to the expression of GAPDH . Data was normalized to a vehicle control ( N = 5). K, The levels of indicated proteins in similarly treated mice were determined by immunoblotting from a cohort of vehicle (1–5) or SSTC3 (6–10)-treated mice. L, Two-month-old ND2:SMOA1 mice were treated with SSTC3 (10 mg/kg i.p. in DMSO) every other day for 1 month and medulloblastoma symptom-free survival monitored for 9 additional months ( N = 10).

    Techniques Used: Derivative Assay, Gel Permeation Chromatography, BrdU Incorporation Assay, Mouse Assay, Staining, Biomarker Assay, Immunostaining, Injection, Expressing

    12) Product Images from "Multipotent luminal mammary cancer stem cells model tumor heterogeneity"

    Article Title: Multipotent luminal mammary cancer stem cells model tumor heterogeneity

    Journal: Breast Cancer Research : BCR

    doi: 10.1186/s13058-015-0615-y

    MaCSCs have the capacity to differentiate into multiple cell types. ( a ) A single Py230 cell stained with myoepithelial marker keratin 14 (K14) and luminal marker keratin 8 (K8). ( b ) Clonal Py230 cells grown on a glass coverslip stained with K14 and K8. Scale bar 20 μm. ( c ) Clonogenic efficiency of C57Bl/6 MaCSC line Py230 and FVB/N MaCSC line Py9813. ( d ) Hollow mammospheres of Py230 cells in suspension culture. Scale bar 50 μm. ( e,f ) Py230 mammosphere stained with K14 and K8. Scale bar 20 μm. ( g ) Py230 mammosphere grown on collagen exhibits branching structures. Scale bar 100 μm. ( h ) Confluent Py230 cells spontaneously form domes. ( i ) Domes become enlarged upon treatment with lactogenic hormones dexamethasone and prolactin. Scale bar 50 μm. ( j ) Expression of beta-casein by MaCSC lines Py230 and Py9813 following treatment with lactogenic hormones. Data are means ± SEM of triplicate samples. ( k ) Py230 cells treated with retinoic acid and rosiglitazone express genes associated with adipocyte differentiation. Data are means ± SEM of triplicate samples. Inset: Py230 cells stained with oil red O. Scale bar 10 μm
    Figure Legend Snippet: MaCSCs have the capacity to differentiate into multiple cell types. ( a ) A single Py230 cell stained with myoepithelial marker keratin 14 (K14) and luminal marker keratin 8 (K8). ( b ) Clonal Py230 cells grown on a glass coverslip stained with K14 and K8. Scale bar 20 μm. ( c ) Clonogenic efficiency of C57Bl/6 MaCSC line Py230 and FVB/N MaCSC line Py9813. ( d ) Hollow mammospheres of Py230 cells in suspension culture. Scale bar 50 μm. ( e,f ) Py230 mammosphere stained with K14 and K8. Scale bar 20 μm. ( g ) Py230 mammosphere grown on collagen exhibits branching structures. Scale bar 100 μm. ( h ) Confluent Py230 cells spontaneously form domes. ( i ) Domes become enlarged upon treatment with lactogenic hormones dexamethasone and prolactin. Scale bar 50 μm. ( j ) Expression of beta-casein by MaCSC lines Py230 and Py9813 following treatment with lactogenic hormones. Data are means ± SEM of triplicate samples. ( k ) Py230 cells treated with retinoic acid and rosiglitazone express genes associated with adipocyte differentiation. Data are means ± SEM of triplicate samples. Inset: Py230 cells stained with oil red O. Scale bar 10 μm

    Techniques Used: Staining, Marker, Expressing

    13) Product Images from "Functionally Distinct Subgroups of Oligodendrocyte Precursor Cells Integrate Neural Activity and Execute Myelin Formation"

    Article Title: Functionally Distinct Subgroups of Oligodendrocyte Precursor Cells Integrate Neural Activity and Execute Myelin Formation

    Journal: Nature neuroscience

    doi: 10.1038/s41593-019-0581-2

    Effects of chronic 4-AP incubation on zebrafish. a) Minimum intensity projections of a two-minute time-lapse of fish freely swimming in a 3 cm petri dish in different treatment conditions (n=6/7/3/3 animals in control/4-AP/TTX/4-AP+TTX, 3 independent experiments). b) Traces of GCaMP transients Tg(elavl3:h2b-GCaMP6s) zebrafish at 4 dpf and after overnight incubation in 0.1 mM 4-AP, and before / after 10 μM TTX (7 animals per conditions in 2 experiments). c) Confocal images of Tg(mfap4:memCerulean), Tg(olig1:nls-mApple) zebrafish at 4 dpf after treatment with 0.1 mM 4-AP, 0.5 mM 4-AP, or Danieau’s solution as control. Transmitted light images to show spinal cord morphology and tissue integrity following drug treatment. Scale bars: 100 μm. The graph shows that number of macrophages which accumulate in 400 μM length of spinal cord of Tg(mfap4:memCerulean) zebrafish after 1 day of control (2±0.25/2 cells), 0.1 mM (2±1/2 cells), and 0.5 mM (3±0.25/2 cells) 4-AP treatment (median (25%/75% percentiles); p=0.43 (control vs . 0.1mM 4-AP), p=0.03 (control vs. 0.5 mM 4-AP) (Kruskal-Wallis test, test statistic=3.003), n=16/19/8 animals in 3 experiments. d) Representative images of Tg(mbp:nls-EGFP), Tg(olig1:nls-mApple) zebrafish in control and after 2 days of 0.1 mM 4-AP treatment (see for n numbers). Scale bar: 20 μm. Fig 7g
    Figure Legend Snippet: Effects of chronic 4-AP incubation on zebrafish. a) Minimum intensity projections of a two-minute time-lapse of fish freely swimming in a 3 cm petri dish in different treatment conditions (n=6/7/3/3 animals in control/4-AP/TTX/4-AP+TTX, 3 independent experiments). b) Traces of GCaMP transients Tg(elavl3:h2b-GCaMP6s) zebrafish at 4 dpf and after overnight incubation in 0.1 mM 4-AP, and before / after 10 μM TTX (7 animals per conditions in 2 experiments). c) Confocal images of Tg(mfap4:memCerulean), Tg(olig1:nls-mApple) zebrafish at 4 dpf after treatment with 0.1 mM 4-AP, 0.5 mM 4-AP, or Danieau’s solution as control. Transmitted light images to show spinal cord morphology and tissue integrity following drug treatment. Scale bars: 100 μm. The graph shows that number of macrophages which accumulate in 400 μM length of spinal cord of Tg(mfap4:memCerulean) zebrafish after 1 day of control (2±0.25/2 cells), 0.1 mM (2±1/2 cells), and 0.5 mM (3±0.25/2 cells) 4-AP treatment (median (25%/75% percentiles); p=0.43 (control vs . 0.1mM 4-AP), p=0.03 (control vs. 0.5 mM 4-AP) (Kruskal-Wallis test, test statistic=3.003), n=16/19/8 animals in 3 experiments. d) Representative images of Tg(mbp:nls-EGFP), Tg(olig1:nls-mApple) zebrafish in control and after 2 days of 0.1 mM 4-AP treatment (see for n numbers). Scale bar: 20 μm. Fig 7g

    Techniques Used: Incubation, Fluorescence In Situ Hybridization

    Related Articles

    Centrifugation:

    Article Title: Highly active antiretroviral therapy dysregulates proliferation and differentiation of human pre-adipocytes
    Article Snippet: .. In brief, fat tissue was digested with collagenase (3 mg/mL, type II, Worthington, Lakewood, NJ) to obtain stromal cells that were then separated from mature adipocytes by centrifugation and incubated in erythrocyte lysing buffer (154 mmol/L NH4 Cl, 10 mmol/L K2 HPO4 , 1 mmol/L EDTA, pH 7.4) for 10 min at room temperature to eliminate red cells. ..

    Cell Isolation:

    Article Title: p38? Negatively Regulates Survival and Malignant Selection of Transformed Bronchioalveolar Stem Cells
    Article Snippet: .. Cell Isolation and Cell Culture Mouse lung tissues from wild-type or LSL-K-rasG12D –TetO-sftpc-Cre C57BL/6 mice were disassociated by finely mincing with a razor blade and by incubating in Dulbecco’s modified Eagle’s medium (DMEM, PAA) containing collagenase (3 mg/mL, Worthington Biochemical) for 30 minutes at 37°C in a shaking incubator. ..

    Cell Culture:

    Article Title: p38? Negatively Regulates Survival and Malignant Selection of Transformed Bronchioalveolar Stem Cells
    Article Snippet: .. Cell Isolation and Cell Culture Mouse lung tissues from wild-type or LSL-K-rasG12D –TetO-sftpc-Cre C57BL/6 mice were disassociated by finely mincing with a razor blade and by incubating in Dulbecco’s modified Eagle’s medium (DMEM, PAA) containing collagenase (3 mg/mL, Worthington Biochemical) for 30 minutes at 37°C in a shaking incubator. ..

    Mouse Assay:

    Article Title: p38? Negatively Regulates Survival and Malignant Selection of Transformed Bronchioalveolar Stem Cells
    Article Snippet: .. Cell Isolation and Cell Culture Mouse lung tissues from wild-type or LSL-K-rasG12D –TetO-sftpc-Cre C57BL/6 mice were disassociated by finely mincing with a razor blade and by incubating in Dulbecco’s modified Eagle’s medium (DMEM, PAA) containing collagenase (3 mg/mL, Worthington Biochemical) for 30 minutes at 37°C in a shaking incubator. ..

    Incubation:

    Article Title: Highly active antiretroviral therapy dysregulates proliferation and differentiation of human pre-adipocytes
    Article Snippet: .. In brief, fat tissue was digested with collagenase (3 mg/mL, type II, Worthington, Lakewood, NJ) to obtain stromal cells that were then separated from mature adipocytes by centrifugation and incubated in erythrocyte lysing buffer (154 mmol/L NH4 Cl, 10 mmol/L K2 HPO4 , 1 mmol/L EDTA, pH 7.4) for 10 min at room temperature to eliminate red cells. ..

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    Modification:

    Article Title: p38? Negatively Regulates Survival and Malignant Selection of Transformed Bronchioalveolar Stem Cells
    Article Snippet: .. Cell Isolation and Cell Culture Mouse lung tissues from wild-type or LSL-K-rasG12D –TetO-sftpc-Cre C57BL/6 mice were disassociated by finely mincing with a razor blade and by incubating in Dulbecco’s modified Eagle’s medium (DMEM, PAA) containing collagenase (3 mg/mL, Worthington Biochemical) for 30 minutes at 37°C in a shaking incubator. ..

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    Worthington Biochemical acta2 rfpcherry tg mice
    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions <t>Lyz2-EGFP-ki;Acta2-RFPcherry-Tg</t> mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
    Acta2 Rfpcherry Tg Mice, supplied by Worthington Biochemical, used in various techniques. Bioz Stars score: 92/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions <t>Lyz2-EGFP-ki;Acta2-RFPcherry-Tg</t> mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
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    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions <t>Lyz2-EGFP-ki;Acta2-RFPcherry-Tg</t> mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p
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    Image Search Results


    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Journal: Immunity

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    doi: 10.1016/j.immuni.2018.09.018

    Figure Lengend Snippet: TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). (E) Time-lapse IVM images ( Video S1 ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). (G) IVM images ( Video S2 ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Article Snippet: Pericyte isolation and culture Cremaster muscles from Acta2-RFPcherry-Tg mice were digested with 500 U/mL Collagenase II (Worthington) in PBS for 45 min at 37°C and 50 U/mL DNase I (Sigma-Aldrich) was added during the last 20 min.

    Techniques: Mouse Assay, In Vivo, Labeling, Blocking Assay, Injection, Transmission Electron Microscopy

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Journal: Immunity

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    doi: 10.1016/j.immuni.2018.09.018

    Figure Lengend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. (C) Time-lapse IVM images ( Video S3 ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). (H) Time-lapse confocal IVM images ( Video S4 ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Article Snippet: Pericyte isolation and culture Cremaster muscles from Acta2-RFPcherry-Tg mice were digested with 500 U/mL Collagenase II (Worthington) in PBS for 45 min at 37°C and 50 U/mL DNase I (Sigma-Aldrich) was added during the last 20 min.

    Techniques: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition

    TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Journal: Immunity

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    doi: 10.1016/j.immuni.2018.09.018

    Figure Lengend Snippet: TNF-Elicited CXCL1 and CXCL2 Support Distinct Phases of Neutrophil-EC Interactions Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were treated with ctr or blocking mAbs (i.v. 10 min prior to TNF in C and D and i.s. 100 min post TNF in E–H) and neutrophil responses in cremaster muscles injected locally with PBS or TNF quantified by confocal IVM. (A) Illustrative images of the employed IVM model (scale bar, 20 μm). (B) Scheme depicting neutrophil responses quantified in (C)–(H). (C and D) Quantification of neutrophil adhesion and intraluminal crawling (n = 5–6 mice per group, 23 independent experiments). ) of a neutrophil TEM response in a TNF-stimulated tissue showing a neutrophil migrating from the lumen (0 min) through an EC junction (2–4 min) into the sub-EC space (6 min). Representative of 11 independent experiments; cross sections, top; luminal views, bottom; scale bars, 5 μm. (F) Quantifications of neutrophil TEM (n = 4–11 mice per group, 27 independent experiments). ) of an aborted TEM response in a mouse treated with local TNF+anti-CXCL2 mAb. The images show a luminal neutrophil extending a protrusion through an EC junction (1 min), retracting the protrusion, and re-entering the circulation (5–8 min). Representative of 6 independent experiments; cross sections and luminal views; scale bars, 5 μm. (H) Quantification of aborted neutrophil TEM (n = 4–11 mice per group, 21 independent experiments). Means ± SEM, ∗ p

    Article Snippet: Cremaster muscles from Acta2-RFPcherry-Tg mice were digested with 500 U/mL Collagenase II (Worthington) in PBS for 45 min at 37°C and 50 U/mL DNase I (Sigma-Aldrich) was added during the last 20 min.

    Techniques: Mouse Assay, In Vivo, Labeling, Blocking Assay, Injection, Transmission Electron Microscopy

    Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Journal: Immunity

    Article Title: Distinct Compartmentalization of the Chemokines CXCL1 and CXCL2 and the Atypical Receptor ACKR1 Determine Discrete Stages of Neutrophil Diapedesis

    doi: 10.1016/j.immuni.2018.09.018

    Figure Lengend Snippet: Neutrophil-Pericyte Interactions Are Selectively Mediated by Endogenous CXCL1 Lyz2-EGFP-ki;Acta2-RFPcherry-Tg mice, subjected to in vivo CD31 labeling, were stimulated locally with TNF and 100 min later i.s. injected with ctr or blocking mAbs, as indicated. (A) Neutrophil responses quantified in cremasteric venules by confocal IVM in (C)–(G). (B) Representative confocal IVM luminal and cross-sectional views depicting a neutrophil localized between TNF-stimulated ECs and pericytes 1 min post TEM. ) showing a neutrophil crawling on pericytes (tracks, dashed lines) in a TNF-stimulated tissue (top) and the inhibition of this response in tissues treated with anti-CXCL1 mAb (bottom). Scale bars in (B) and (C), 10 μm. (D–G) Crawling profiles of neutrophils on pericytes (20 cells per group for clarity) (D) as normalized for their origin and associated quantifications of displacement (E), straightness index (displacement/track length) (F), and breaching of the pericyte layer (G). ) illustrating neutrophil reverse TEM in a tissue treated with TNF+anti-CXCL1 mAb (luminal and cross-sectional views; scale bars, 5 μm). (I) Quantifications of neutrophil reverse TEM. Images are representative of 5–10 independent experiments and quantifications (n = 5–10 mice per group) involve 20 independent experiments.

    Article Snippet: Cremaster muscles from Acta2-RFPcherry-Tg mice were digested with 500 U/mL Collagenase II (Worthington) in PBS for 45 min at 37°C and 50 U/mL DNase I (Sigma-Aldrich) was added during the last 20 min.

    Techniques: Mouse Assay, In Vivo, Labeling, Injection, Blocking Assay, Transmission Electron Microscopy, Inhibition