huh7 5 cells  (ATCC)


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    Structured Review

    ATCC huh7 5 cells
    CSMut1 design, modelling and infectivity. ( a ) The wild type E 250–270 and CSMut1 sequences are shown with mutated amino acids highlighted in red. ( b ) Wild type (on the left) and CSMut1 model (on the right) with E 250–270 in red. ( c ) Relative quantification of DV NS5 RNA in <t>Huh7.5</t> cells transfected with wild type and CSMut1 genomes at different time points. Cell associated RNA is shown in the left panel and supernatant extracted RNA in the right panel. ( d ) DV E-protein immunofluorescence staining of WT and CSMut1 120 hours after genome transfection in Huh7.5 cells (bars correspond to 32 μM).
    Huh7 5 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 3 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Genome-wide analyses reveal a highly conserved Dengue virus envelope peptide which is critical for virus viability and antigenic in humans"

    Article Title: Genome-wide analyses reveal a highly conserved Dengue virus envelope peptide which is critical for virus viability and antigenic in humans

    Journal: Scientific Reports

    doi: 10.1038/srep36339

    CSMut1 design, modelling and infectivity. ( a ) The wild type E 250–270 and CSMut1 sequences are shown with mutated amino acids highlighted in red. ( b ) Wild type (on the left) and CSMut1 model (on the right) with E 250–270 in red. ( c ) Relative quantification of DV NS5 RNA in Huh7.5 cells transfected with wild type and CSMut1 genomes at different time points. Cell associated RNA is shown in the left panel and supernatant extracted RNA in the right panel. ( d ) DV E-protein immunofluorescence staining of WT and CSMut1 120 hours after genome transfection in Huh7.5 cells (bars correspond to 32 μM).
    Figure Legend Snippet: CSMut1 design, modelling and infectivity. ( a ) The wild type E 250–270 and CSMut1 sequences are shown with mutated amino acids highlighted in red. ( b ) Wild type (on the left) and CSMut1 model (on the right) with E 250–270 in red. ( c ) Relative quantification of DV NS5 RNA in Huh7.5 cells transfected with wild type and CSMut1 genomes at different time points. Cell associated RNA is shown in the left panel and supernatant extracted RNA in the right panel. ( d ) DV E-protein immunofluorescence staining of WT and CSMut1 120 hours after genome transfection in Huh7.5 cells (bars correspond to 32 μM).

    Techniques Used: Infection, Transfection, Immunofluorescence, Staining

    2) Product Images from "IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer"

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    Journal: Molecular Medicine Reports

    doi: 10.3892/mmr.2019.10310

    IL-17A upregulates the production of pro-angiogenic CXC chemokines in liver cancer cells. The effect of IL-17A overexpression on the expression levels of angiogenic factors in (A) Huh7.5 and (B) HepG2 cells was determined by RT-qPCR. *P
    Figure Legend Snippet: IL-17A upregulates the production of pro-angiogenic CXC chemokines in liver cancer cells. The effect of IL-17A overexpression on the expression levels of angiogenic factors in (A) Huh7.5 and (B) HepG2 cells was determined by RT-qPCR. *P

    Techniques Used: Over Expression, Expressing, Quantitative RT-PCR

    Expression of IL17RA and VEGFR2 in liver cancer-derived cell lines. The expression of IL17RA and VEGFR2 in HepG2 and Huh7.5 cells was examined by reverse transcription-quantitative PCR. GAPDH served as the internal control. **P
    Figure Legend Snippet: Expression of IL17RA and VEGFR2 in liver cancer-derived cell lines. The expression of IL17RA and VEGFR2 in HepG2 and Huh7.5 cells was examined by reverse transcription-quantitative PCR. GAPDH served as the internal control. **P

    Techniques Used: Expressing, Derivative Assay, Real-time Polymerase Chain Reaction

    IL-17A has no effect on the proliferation of liver cancer cells. (A) HepG2 and Huh7.5 cells overexpressing EGFP or IL-17A were cultured in 6-well plates for 24 h. The concentration of IL-17A in the cell-free supernatants was measured by IL-17A ELISA. **P
    Figure Legend Snippet: IL-17A has no effect on the proliferation of liver cancer cells. (A) HepG2 and Huh7.5 cells overexpressing EGFP or IL-17A were cultured in 6-well plates for 24 h. The concentration of IL-17A in the cell-free supernatants was measured by IL-17A ELISA. **P

    Techniques Used: Cell Culture, Concentration Assay, Enzyme-linked Immunosorbent Assay

    Effect of IL-17A on liver cancer cell-induced endothelial cell chemotaxis. The chemotaxis effect of the supernatants from liver cancer cells on HUVEC invasion was examined by Transwell assays. The effect of IL-17A overexpression in (A and C) Huh7.5 or (B and D) HepG2 cells on endothelial cell chemotaxis. Antibody against IL17RA (5 µg/ml) was added during liver cancer cell culture. Chemokine (C-X-C motif) receptor 2 inhibitor SB225002 was added to the supernatants from Huh7.5-EGFP or Huh7.5-IL17A. (A, B and E) Representative 4′,6-diamidino-2-phenylindole staining images of migrated HUVEC are presented and (C, D and F) the calculated values are shown. Data were derived from three independent experiments. Five randomly selected images (magnification, ×400) were used in the calculation for each well. *P
    Figure Legend Snippet: Effect of IL-17A on liver cancer cell-induced endothelial cell chemotaxis. The chemotaxis effect of the supernatants from liver cancer cells on HUVEC invasion was examined by Transwell assays. The effect of IL-17A overexpression in (A and C) Huh7.5 or (B and D) HepG2 cells on endothelial cell chemotaxis. Antibody against IL17RA (5 µg/ml) was added during liver cancer cell culture. Chemokine (C-X-C motif) receptor 2 inhibitor SB225002 was added to the supernatants from Huh7.5-EGFP or Huh7.5-IL17A. (A, B and E) Representative 4′,6-diamidino-2-phenylindole staining images of migrated HUVEC are presented and (C, D and F) the calculated values are shown. Data were derived from three independent experiments. Five randomly selected images (magnification, ×400) were used in the calculation for each well. *P

    Techniques Used: Chemotaxis Assay, Over Expression, Cell Culture, Staining, Derivative Assay

    Overexpression of IL-17A promotes Huh7.5 tumor growth in vivo . Representative tumors from a (A and B) subcutaneous model (n=6) and (C and D) liver model (n=5) are presented; (A and C) Huh7.5-EGFP and (Band D) Huh7.5-IL17A. Scale bar, 5 mm. (E) The tumor volumes of Huh7.5-EGFP and Huh7.5-IL17A tumors in the subcutaneous model were measured at the time-points indicated, and (F) the tumor weights are shown. Data are presented as the mean ± SD. **P
    Figure Legend Snippet: Overexpression of IL-17A promotes Huh7.5 tumor growth in vivo . Representative tumors from a (A and B) subcutaneous model (n=6) and (C and D) liver model (n=5) are presented; (A and C) Huh7.5-EGFP and (Band D) Huh7.5-IL17A. Scale bar, 5 mm. (E) The tumor volumes of Huh7.5-EGFP and Huh7.5-IL17A tumors in the subcutaneous model were measured at the time-points indicated, and (F) the tumor weights are shown. Data are presented as the mean ± SD. **P

    Techniques Used: Over Expression, In Vivo

    Overexpression of IL-17A promotes growth and angiogenesis in Huh7.5 orthotopic tumors. The morphology of Huh7.5-EGFP- or Huh7.5-IL17A-derived liver tumors was examined by (A and B) hematoxylin and eosin staining, and (C and D) the blood vessels were observed via CD31 immunohistochemistry. Scale bar, 50 µm. (E) Quantitative analysis of the immunostaining-positive area in C D. Data are presented as the mean ± SD. **P
    Figure Legend Snippet: Overexpression of IL-17A promotes growth and angiogenesis in Huh7.5 orthotopic tumors. The morphology of Huh7.5-EGFP- or Huh7.5-IL17A-derived liver tumors was examined by (A and B) hematoxylin and eosin staining, and (C and D) the blood vessels were observed via CD31 immunohistochemistry. Scale bar, 50 µm. (E) Quantitative analysis of the immunostaining-positive area in C D. Data are presented as the mean ± SD. **P

    Techniques Used: Over Expression, Derivative Assay, Staining, Immunohistochemistry, Immunostaining

    3) Product Images from "Cyclooxgenase-2 is induced by SARS-CoV-2 infection but does not affect viral entry or replication"

    Article Title: Cyclooxgenase-2 is induced by SARS-CoV-2 infection but does not affect viral entry or replication

    Journal: bioRxiv

    doi: 10.1101/2020.09.24.312769

    NSAID treatment does not affect SARS-CoV-2 entry or replication (A-B) Calu-3 (A) and Huh7.5 (B) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with SARS2-VSVpp or G-VSVpp expressing Renilla luciferase. Luminescence was measured at 24 hours post infection (hpi) and normalized to DMSO for each infection. (C-D) Calu-3 (C) and Huh7.5 (D) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with mNeonGreen reporter replication-competent SARS-CoV-2 (icSARS-CoV-2-mNG) at a MOI of 1. Frequency of infected cells was measured by mNeonGreen expression at 1, 2, and 3 dpi. All data points in this figure are presented as mean ± SEM. Data were analyzed by Student’s two-tailed, unpaired t -test (A-B) and two-way ANOVA (C-D). ns, not significant. Data in (A-B) are representative of two independent experiments with four replicates per condition. Data in (C-D) are representative of two independent experiments with five replicates per condition.
    Figure Legend Snippet: NSAID treatment does not affect SARS-CoV-2 entry or replication (A-B) Calu-3 (A) and Huh7.5 (B) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with SARS2-VSVpp or G-VSVpp expressing Renilla luciferase. Luminescence was measured at 24 hours post infection (hpi) and normalized to DMSO for each infection. (C-D) Calu-3 (C) and Huh7.5 (D) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with mNeonGreen reporter replication-competent SARS-CoV-2 (icSARS-CoV-2-mNG) at a MOI of 1. Frequency of infected cells was measured by mNeonGreen expression at 1, 2, and 3 dpi. All data points in this figure are presented as mean ± SEM. Data were analyzed by Student’s two-tailed, unpaired t -test (A-B) and two-way ANOVA (C-D). ns, not significant. Data in (A-B) are representative of two independent experiments with four replicates per condition. Data in (C-D) are representative of two independent experiments with five replicates per condition.

    Techniques Used: Infection, Expressing, Luciferase, Two Tailed Test

    SARS-CoV-2 infection induces PTGS2 expression in human and mouse systems (A) Calu-3 cells were infected with SARS-CoV-2 at a multiplicity of infection (MOI) of 0.05. PTGS2 expression was measured at 2 days post infection (dpi), normalized to ACTB . (B-C) PTGS2 expression in Calu-3 (B) and ACE2-overexpressing A549 (A549-ACE2) (C) cells following SARS-CoV-2 infection. Data are from GSE147507 (Blanco-Melo et al., 2020). (D) Huh7.5 cells were infected with SARS-CoV-2 at a MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (E) Human bronchial epithelial cells (HBECs) were cultured at an air-liquid interface and then infected at the apical surface with 10 4 plaque-forming units (PFU) of SARS-CoV-2. Cells were collected at 1, 2, and 3 dpi for single-cell RNA sequencing (scRNA-seq) ( 16 ). Volcano plot of differentially expressed genes in infected versus bystander ciliated cells pooled from all time points. PTGS2 is highlighted. (F) K18-hACE2 mice were infected intranasally with 1.2 × 10 6 PFU of SARS-CoV-2. Ptgs2 expression in the lung was measured at 0, 2, 4, and 7 dpi. (G) Ptgs2 expression in the lung of K18-hACE2 mice following intranasal SARS-CoV-2 infection. Data are from GSE154104 (Winkler et al., 2020). All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (A, D, F); Student’s two-tailed, unpaired t -test (B, C, G); and two-sided Mann-Whitney U test with continuity and Benjamini-Hochberg correction (E). *P
    Figure Legend Snippet: SARS-CoV-2 infection induces PTGS2 expression in human and mouse systems (A) Calu-3 cells were infected with SARS-CoV-2 at a multiplicity of infection (MOI) of 0.05. PTGS2 expression was measured at 2 days post infection (dpi), normalized to ACTB . (B-C) PTGS2 expression in Calu-3 (B) and ACE2-overexpressing A549 (A549-ACE2) (C) cells following SARS-CoV-2 infection. Data are from GSE147507 (Blanco-Melo et al., 2020). (D) Huh7.5 cells were infected with SARS-CoV-2 at a MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (E) Human bronchial epithelial cells (HBECs) were cultured at an air-liquid interface and then infected at the apical surface with 10 4 plaque-forming units (PFU) of SARS-CoV-2. Cells were collected at 1, 2, and 3 dpi for single-cell RNA sequencing (scRNA-seq) ( 16 ). Volcano plot of differentially expressed genes in infected versus bystander ciliated cells pooled from all time points. PTGS2 is highlighted. (F) K18-hACE2 mice were infected intranasally with 1.2 × 10 6 PFU of SARS-CoV-2. Ptgs2 expression in the lung was measured at 0, 2, 4, and 7 dpi. (G) Ptgs2 expression in the lung of K18-hACE2 mice following intranasal SARS-CoV-2 infection. Data are from GSE154104 (Winkler et al., 2020). All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (A, D, F); Student’s two-tailed, unpaired t -test (B, C, G); and two-sided Mann-Whitney U test with continuity and Benjamini-Hochberg correction (E). *P

    Techniques Used: Infection, Expressing, Cell Culture, RNA Sequencing Assay, Mouse Assay, Two Tailed Test, MANN-WHITNEY

    NSAID treatment does not affect ACE2 expression in human cell lines (A-B) Calu-3 (A) and Huh7.5 (B) cells were treated with different concentrations of ibuprofen or meloxicam for 48 hours. Cell viability was measured and calculated as a percentage of no treatment. (C) Calu-3 cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 48 hours. Levels of prostaglandin E 2 (PGE 2 ) were measured in the supernatant. Dotted line represents limit of detection. (D-E) Calu-3 (D) and Huh7.5 (E) cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours. ACE2 expression was measured and normalized to ACTB . All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (C-E). **P
    Figure Legend Snippet: NSAID treatment does not affect ACE2 expression in human cell lines (A-B) Calu-3 (A) and Huh7.5 (B) cells were treated with different concentrations of ibuprofen or meloxicam for 48 hours. Cell viability was measured and calculated as a percentage of no treatment. (C) Calu-3 cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 48 hours. Levels of prostaglandin E 2 (PGE 2 ) were measured in the supernatant. Dotted line represents limit of detection. (D-E) Calu-3 (D) and Huh7.5 (E) cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours. ACE2 expression was measured and normalized to ACTB . All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (C-E). **P

    Techniques Used: Expressing, Two Tailed Test

    4) Product Images from "Functional innate immunity restricts Hepatitis C Virus infection in induced pluripotent stem cell–derived hepatocytes"

    Article Title: Functional innate immunity restricts Hepatitis C Virus infection in induced pluripotent stem cell–derived hepatocytes

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-22243-7

    Immature and mature iHLCs are permissive to HCV infection. ( a ) Scheme of the experimental setup. ( b ) Permissivity at different stages of differentiation. Cells were infected with cell culture derived Jc1 p7-GLuc-2A-NS2 from day 12–20 of differentiation and viral replication was monitored for 7 days. 24 h post infection, cells were washed and the last wash was kept as T = 0. Gaussia luciferase activity was measured in the supernatant and in the washes after media change at the indicated time points. The dashed horizontal line represents the background luciferase activity determined in mock-infected iHLCs. ( c ) Re-infection of Huh7.5 cells with supernatant collected during ( b ). Huh7.5 cells were infected with the iHLC supernatant from T = 1–5 to determine the production of infectious viral particles at different stages of differentiation. Gaussia luciferase activity was measured 2 days post re-infection (Mean ± SD, duplicate measurements). The dashed horizontal line represents the background luciferase activity determined in mock-infected Huh7.5 cells.
    Figure Legend Snippet: Immature and mature iHLCs are permissive to HCV infection. ( a ) Scheme of the experimental setup. ( b ) Permissivity at different stages of differentiation. Cells were infected with cell culture derived Jc1 p7-GLuc-2A-NS2 from day 12–20 of differentiation and viral replication was monitored for 7 days. 24 h post infection, cells were washed and the last wash was kept as T = 0. Gaussia luciferase activity was measured in the supernatant and in the washes after media change at the indicated time points. The dashed horizontal line represents the background luciferase activity determined in mock-infected iHLCs. ( c ) Re-infection of Huh7.5 cells with supernatant collected during ( b ). Huh7.5 cells were infected with the iHLC supernatant from T = 1–5 to determine the production of infectious viral particles at different stages of differentiation. Gaussia luciferase activity was measured 2 days post re-infection (Mean ± SD, duplicate measurements). The dashed horizontal line represents the background luciferase activity determined in mock-infected Huh7.5 cells.

    Techniques Used: Infection, Cell Culture, Derivative Assay, Luciferase, Activity Assay

    Induction of ISG expression after HCV infection is stronger in iHLCs compared to hepatoma cells. ( a ) mRNA expression levels of interferon stimulated genes (ISGs) in iHLCs, Huh7.5, and Huh7 cells were determined by qRT-PCR at day 1, 2, and 3 days post infection (dpi) with cell culture–derived HCV (fresh concentrate of Jc1/JFH1 for iHLCs; Jc1 (MOI = 0.01) for Huh7 and Huh7.5). Shown are expression levels relative to GAPDH (mean ± SEM, n = 2–3). ( b ) Induction of ISGs in iHLCs after HCV infection as log 2 -fold over uninfected control (normalised to GAPDH , mean ± SEM, n = 3, * p
    Figure Legend Snippet: Induction of ISG expression after HCV infection is stronger in iHLCs compared to hepatoma cells. ( a ) mRNA expression levels of interferon stimulated genes (ISGs) in iHLCs, Huh7.5, and Huh7 cells were determined by qRT-PCR at day 1, 2, and 3 days post infection (dpi) with cell culture–derived HCV (fresh concentrate of Jc1/JFH1 for iHLCs; Jc1 (MOI = 0.01) for Huh7 and Huh7.5). Shown are expression levels relative to GAPDH (mean ± SEM, n = 2–3). ( b ) Induction of ISGs in iHLCs after HCV infection as log 2 -fold over uninfected control (normalised to GAPDH , mean ± SEM, n = 3, * p

    Techniques Used: Expressing, Infection, Quantitative RT-PCR, Cell Culture, Derivative Assay

    Differentiation and characteristics of iHLCs. ( a ) Cell morphology and culture conditions at different stages of differentiation from iPSCs into iHLCs. Bright-field images were taken at the indicated time points (scale bar 100 µm). ( b ) Sequential expression and repression of transcription factors marking successful differentiation. Cells were immunostained with antibodies against Oct 3/4 (pluripotency marker), the endodermal transcription factor GATA-4, and the hepatic marker HNF4α at day 0, 5, and 10 of differentiation (scale bars 20 µm). Shown are representative fluorescence and DIC images. ( c ) mRNA expression levels of different hepatocyte-specific factors in iHLCs, Huh7.5 cells, and primary human hepatocytes (PHHs) were analysed via qRT-PCR. Expression levels are displayed as fold over iPSCs normalised to GAPDH and 18S rRNA (mean ± SEM, n = 3–4, * p
    Figure Legend Snippet: Differentiation and characteristics of iHLCs. ( a ) Cell morphology and culture conditions at different stages of differentiation from iPSCs into iHLCs. Bright-field images were taken at the indicated time points (scale bar 100 µm). ( b ) Sequential expression and repression of transcription factors marking successful differentiation. Cells were immunostained with antibodies against Oct 3/4 (pluripotency marker), the endodermal transcription factor GATA-4, and the hepatic marker HNF4α at day 0, 5, and 10 of differentiation (scale bars 20 µm). Shown are representative fluorescence and DIC images. ( c ) mRNA expression levels of different hepatocyte-specific factors in iHLCs, Huh7.5 cells, and primary human hepatocytes (PHHs) were analysed via qRT-PCR. Expression levels are displayed as fold over iPSCs normalised to GAPDH and 18S rRNA (mean ± SEM, n = 3–4, * p

    Techniques Used: Expressing, Marker, Fluorescence, Quantitative RT-PCR

    5) Product Images from "Differential Induction of Immunogenic Cell Death and Interferon Expression in Cancer Cells by Structured ssRNAs"

    Article Title: Differential Induction of Immunogenic Cell Death and Interferon Expression in Cancer Cells by Structured ssRNAs

    Journal: Molecular Therapy

    doi: 10.1016/j.ymthe.2017.03.014

    Induction of RNA-Sensing PRR-Mediated Cytotoxicity by ICR2 and ICR4 (A) Huh7.0 (RIG-I wild-type) and Huh7.5 (RIG-I mutant) cells (7 × 10 3 cells/well) were transfected with ICR2 or ICR4 (1 μg/mL each) or mock-transfected in a 96-well plate. Cytotoxicity was determined 3 days after transfection by MTS assay. (B) RIG-I, PKR, and MDA5 in WM266-4 cells were knocked down three times with siRNAs. Cells (1 × 10 4 cells/well) were re-plated in a 96-well plate and transfected with ICR2 or ICR4 (0.2 μg/mL each) or mock-transfected. Cytotoxicity was determined 3 days after transfection by MTS assay. (C) Knockdown of RIG-I, MDA5, and PKR in human melanoma cells. siRNA-mediated knockdown efficiency was assessed 4 days after mock transfections (control) or siRNA (lacking 5′ppp) transfections by western blot using siRNA-corresponding antibodies as indicated. β-Actin antibody was used as a loading control. (D) HEK-TLR3 and HEK-TLR7 reporter cells (4 × 10 4 cells/well each) were transfected with ICR2, ICR4 or poly(I:C) (pIC) (0.5 μg/mL each). Non-transfected poly(I:C) and R848 were used as positive controls for TLR3 and TLR7, respectively. PBS treatment was used as a negative control. (E and F) ICR2 and ICR4 were dephosphorylated by treatment with a BAP. The dephosphorylation was repeated twice. WM266-4 cells were transfected with BAP-treated and BAP-untreated ICR2 or ICR4 (30 nM each) or mock transfection. Cytotoxicity and IFN-β production was determined 2 days after transfection. Error bar represent SD. *p
    Figure Legend Snippet: Induction of RNA-Sensing PRR-Mediated Cytotoxicity by ICR2 and ICR4 (A) Huh7.0 (RIG-I wild-type) and Huh7.5 (RIG-I mutant) cells (7 × 10 3 cells/well) were transfected with ICR2 or ICR4 (1 μg/mL each) or mock-transfected in a 96-well plate. Cytotoxicity was determined 3 days after transfection by MTS assay. (B) RIG-I, PKR, and MDA5 in WM266-4 cells were knocked down three times with siRNAs. Cells (1 × 10 4 cells/well) were re-plated in a 96-well plate and transfected with ICR2 or ICR4 (0.2 μg/mL each) or mock-transfected. Cytotoxicity was determined 3 days after transfection by MTS assay. (C) Knockdown of RIG-I, MDA5, and PKR in human melanoma cells. siRNA-mediated knockdown efficiency was assessed 4 days after mock transfections (control) or siRNA (lacking 5′ppp) transfections by western blot using siRNA-corresponding antibodies as indicated. β-Actin antibody was used as a loading control. (D) HEK-TLR3 and HEK-TLR7 reporter cells (4 × 10 4 cells/well each) were transfected with ICR2, ICR4 or poly(I:C) (pIC) (0.5 μg/mL each). Non-transfected poly(I:C) and R848 were used as positive controls for TLR3 and TLR7, respectively. PBS treatment was used as a negative control. (E and F) ICR2 and ICR4 were dephosphorylated by treatment with a BAP. The dephosphorylation was repeated twice. WM266-4 cells were transfected with BAP-treated and BAP-untreated ICR2 or ICR4 (30 nM each) or mock transfection. Cytotoxicity and IFN-β production was determined 2 days after transfection. Error bar represent SD. *p

    Techniques Used: Mutagenesis, Transfection, MTS Assay, Western Blot, Negative Control, De-Phosphorylation Assay

    6) Product Images from "RIG-I-Mediated STING Upregulation Restricts Herpes Simplex Virus 1 Infection"

    Article Title: RIG-I-Mediated STING Upregulation Restricts Herpes Simplex Virus 1 Infection

    Journal: Journal of Virology

    doi: 10.1128/JVI.00748-16

    Expression of STING is upregulated upon RIG-I signaling. A549 cells (A, B), IHHs, PC3 cells, U87 cells, Huh7.5 cells, or Huh7 cells (C), Ddx58 +/+ or Ddx58 −/− MEFs (D), and shctl- and shMAVS-transfected A549 cells (F) were uninfected or
    Figure Legend Snippet: Expression of STING is upregulated upon RIG-I signaling. A549 cells (A, B), IHHs, PC3 cells, U87 cells, Huh7.5 cells, or Huh7 cells (C), Ddx58 +/+ or Ddx58 −/− MEFs (D), and shctl- and shMAVS-transfected A549 cells (F) were uninfected or

    Techniques Used: Expressing, Transfection

    7) Product Images from "Nonsteroidal Anti-inflammatory Drugs Dampen the Cytokine and Antibody Response to SARS-CoV-2 Infection"

    Article Title: Nonsteroidal Anti-inflammatory Drugs Dampen the Cytokine and Antibody Response to SARS-CoV-2 Infection

    Journal: Journal of Virology

    doi: 10.1128/JVI.00014-21

    NSAID treatment does not affect ACE2 expression in human cells and mice. (A and B) Calu-3 (A) and Huh7.5 (B) cells were treated with different concentrations of ibuprofen or meloxicam for 48 h. Cell viability was measured and calculated as a percentage of no treatment. (C) Calu-3 cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 48 h. The levels of prostaglandin E 2 (PGE 2 ) were measured in the supernatant. The dotted line represents the limit of detection. (D and E) Calu-3 (D) and Huh7.5 (E) cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 h. ACE2 expression was measured and normalized to ACTB . (F to I) C57BL/6 mice were treated intraperitoneally with DMSO, 30 mg/kg ibuprofen, or 1 mg/kg meloxicam daily for 4 days. Ace2 expression was measured in the lung (F), heart (G), kidney (H), and ileum (I), normalized to Actb . All data points in this figure are presented as means ± the SEM. Data were analyzed by Welch’s two-tailed, unpaired t test (C to I). **, P
    Figure Legend Snippet: NSAID treatment does not affect ACE2 expression in human cells and mice. (A and B) Calu-3 (A) and Huh7.5 (B) cells were treated with different concentrations of ibuprofen or meloxicam for 48 h. Cell viability was measured and calculated as a percentage of no treatment. (C) Calu-3 cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 48 h. The levels of prostaglandin E 2 (PGE 2 ) were measured in the supernatant. The dotted line represents the limit of detection. (D and E) Calu-3 (D) and Huh7.5 (E) cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 h. ACE2 expression was measured and normalized to ACTB . (F to I) C57BL/6 mice were treated intraperitoneally with DMSO, 30 mg/kg ibuprofen, or 1 mg/kg meloxicam daily for 4 days. Ace2 expression was measured in the lung (F), heart (G), kidney (H), and ileum (I), normalized to Actb . All data points in this figure are presented as means ± the SEM. Data were analyzed by Welch’s two-tailed, unpaired t test (C to I). **, P

    Techniques Used: Expressing, Mouse Assay, Two Tailed Test

    NSAID treatment does not affect SARS-CoV-2 entry or replication in vitro . (A and B) Calu-3 (A) and Huh7.5 (B) cells were pretreated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 h and then infected with SARS2-VSVpp or G-VSVpp expressing Renilla luciferase. Luminescence was measured at 24 h postinfection (hpi) and normalized to DMSO for each infection. (C and D) Calu-3 (C) and Huh7.5 (D) cells were pretreated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 h and then infected with mNeonGreen reporter replication-competent SARS-CoV-2 (icSARS-CoV-2-mNG) at an MOI of 1. The frequency of infected cells was measured by mNeonGreen expression at 1, 2, and 3 dpi. All data points in this figure are presented as means ± the SEM. Data were analyzed by Student two-tailed, unpaired t test (A and B) and two-way ANOVA (C and D). ns, not significant. Data in panels A and B are representative of two independent experiments with four replicates per condition; data in panels C and D are representative of two independent experiments with five replicates per condition.
    Figure Legend Snippet: NSAID treatment does not affect SARS-CoV-2 entry or replication in vitro . (A and B) Calu-3 (A) and Huh7.5 (B) cells were pretreated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 h and then infected with SARS2-VSVpp or G-VSVpp expressing Renilla luciferase. Luminescence was measured at 24 h postinfection (hpi) and normalized to DMSO for each infection. (C and D) Calu-3 (C) and Huh7.5 (D) cells were pretreated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 h and then infected with mNeonGreen reporter replication-competent SARS-CoV-2 (icSARS-CoV-2-mNG) at an MOI of 1. The frequency of infected cells was measured by mNeonGreen expression at 1, 2, and 3 dpi. All data points in this figure are presented as means ± the SEM. Data were analyzed by Student two-tailed, unpaired t test (A and B) and two-way ANOVA (C and D). ns, not significant. Data in panels A and B are representative of two independent experiments with four replicates per condition; data in panels C and D are representative of two independent experiments with five replicates per condition.

    Techniques Used: In Vitro, Infection, Expressing, Luciferase, Two Tailed Test

    SARS-CoV-2 infection induces PTGS2 expression in human cells and mice. (A) Calu-3 cells were infected with SARS-CoV-2 at an MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (B and C) PTGS2 expression in Calu-3 (B) and ACE2-overexpressing A549 (A549-ACE2) (C) cells following SARS-CoV-2 infection. The data are from GSE147507 ( 26 ). (D) Huh7.5 cells were infected with SARS-CoV-2 at an MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (E) HBECs were cultured at an air-liquid interface and then infected at the apical surface with 10 4 PFU of SARS-CoV-2. Cells were collected at 1, 2, and 3 dpi for single-cell RNA sequencing (scRNA-seq) ( 28 ). A volcano plot of differentially expressed genes in infected versus bystander ciliated cells pooled from all time points is shown. PTGS2 is highlighted. (F) K18-hACE2 mice were infected intranasally with 1.2 × 10 6 PFU of SARS-CoV-2. Ptgs2 expression in the lung was measured at 0, 2, 4, and 7 dpi. (G) Ptgs2 expression in the lung of K18-hACE2 mice following intranasal SARS-CoV-2 infection. The data are from GSE154104 ( 36 ). All data points in this figure are presented as means ± the standard errors of the mean (SEM). Data were analyzed by Welch’s two-tailed, unpaired t test (A, D, and F); Student two-tailed, unpaired t test (B, C, and G); and two-sided Mann-Whitney U test with continuity and Benjamini-Hochberg correction (E). *, P
    Figure Legend Snippet: SARS-CoV-2 infection induces PTGS2 expression in human cells and mice. (A) Calu-3 cells were infected with SARS-CoV-2 at an MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (B and C) PTGS2 expression in Calu-3 (B) and ACE2-overexpressing A549 (A549-ACE2) (C) cells following SARS-CoV-2 infection. The data are from GSE147507 ( 26 ). (D) Huh7.5 cells were infected with SARS-CoV-2 at an MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (E) HBECs were cultured at an air-liquid interface and then infected at the apical surface with 10 4 PFU of SARS-CoV-2. Cells were collected at 1, 2, and 3 dpi for single-cell RNA sequencing (scRNA-seq) ( 28 ). A volcano plot of differentially expressed genes in infected versus bystander ciliated cells pooled from all time points is shown. PTGS2 is highlighted. (F) K18-hACE2 mice were infected intranasally with 1.2 × 10 6 PFU of SARS-CoV-2. Ptgs2 expression in the lung was measured at 0, 2, 4, and 7 dpi. (G) Ptgs2 expression in the lung of K18-hACE2 mice following intranasal SARS-CoV-2 infection. The data are from GSE154104 ( 36 ). All data points in this figure are presented as means ± the standard errors of the mean (SEM). Data were analyzed by Welch’s two-tailed, unpaired t test (A, D, and F); Student two-tailed, unpaired t test (B, C, and G); and two-sided Mann-Whitney U test with continuity and Benjamini-Hochberg correction (E). *, P

    Techniques Used: Infection, Expressing, Mouse Assay, Cell Culture, RNA Sequencing Assay, Two Tailed Test, MANN-WHITNEY

    8) Product Images from "Extract from Aphloia theiformis, an edible indigenous plant from Reunion Island, impairs Zika virus attachment to the host cell surface"

    Article Title: Extract from Aphloia theiformis, an edible indigenous plant from Reunion Island, impairs Zika virus attachment to the host cell surface

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-29183-2

    A . theiformis extract exerts antiviral effect against 4 DENV clinical isolates and an epidemic Brazilian ZIKV strain. Four DENV serotypes (DENV-1, 2, 3 and 4) and a Brazilian epidemic strain of ZIKV (ZV BR2015/15261) were incubated with A . theiformis extract for 1 h at 37 °C. ( a ) Huh7.5 cells were left uninfected or were infected with DENV at an MOI of 0.1 or with ZIKV at an MOI of 0.4 for 48 h. Recombinant IFN-α 2A (200 IU.mL −1 ) was added 2 h post infection and used as positive control. The percentage of E positive cells was evaluated using the Operetta High-Content Imaging System (PerkinElmer). Results are means ± SD of three independent experiments. ( b ) The residual infectivity of treated particles was titrated in C6/36 cells using a foci-forming immunodetection assay. Data represent the means ± SD from three independent experiments. One-way ANOVA and Dunnett’s test (*p
    Figure Legend Snippet: A . theiformis extract exerts antiviral effect against 4 DENV clinical isolates and an epidemic Brazilian ZIKV strain. Four DENV serotypes (DENV-1, 2, 3 and 4) and a Brazilian epidemic strain of ZIKV (ZV BR2015/15261) were incubated with A . theiformis extract for 1 h at 37 °C. ( a ) Huh7.5 cells were left uninfected or were infected with DENV at an MOI of 0.1 or with ZIKV at an MOI of 0.4 for 48 h. Recombinant IFN-α 2A (200 IU.mL −1 ) was added 2 h post infection and used as positive control. The percentage of E positive cells was evaluated using the Operetta High-Content Imaging System (PerkinElmer). Results are means ± SD of three independent experiments. ( b ) The residual infectivity of treated particles was titrated in C6/36 cells using a foci-forming immunodetection assay. Data represent the means ± SD from three independent experiments. One-way ANOVA and Dunnett’s test (*p

    Techniques Used: Incubation, Infection, Recombinant, Positive Control, Imaging, Immunodetection

    9) Product Images from "Development and effectiveness of Pseudotyped SARS-CoV-2 system as determined by neutralizing efficiency and entry inhibition test in vitro"

    Article Title: Development and effectiveness of Pseudotyped SARS-CoV-2 system as determined by neutralizing efficiency and entry inhibition test in vitro

    Journal: Biosafety and Health

    doi: 10.1016/j.bsheal.2020.08.004

    Screening of sensitive cell lines for pseudotyped SARS-CoV-2 virus infection. (A) Vero, Vero E6, Huh7, and Huh7.5 cells were analyzed to screen the cell line most sensitive to infection by the pseudotyped SARS-CoV-2 system. BHK21 cells were used as the negative control in this system, due to lack of SARS-CoV-2 receptor in the cells.
    Figure Legend Snippet: Screening of sensitive cell lines for pseudotyped SARS-CoV-2 virus infection. (A) Vero, Vero E6, Huh7, and Huh7.5 cells were analyzed to screen the cell line most sensitive to infection by the pseudotyped SARS-CoV-2 system. BHK21 cells were used as the negative control in this system, due to lack of SARS-CoV-2 receptor in the cells.

    Techniques Used: Infection, Negative Control

    10) Product Images from "Nanocurcumin Potently Inhibits SARS-CoV-2 Spike Protein-Induced Cytokine Storm by Deactivation of MAPK/NF-κB Signaling in Epithelial Cells"

    Article Title: Nanocurcumin Potently Inhibits SARS-CoV-2 Spike Protein-Induced Cytokine Storm by Deactivation of MAPK/NF-κB Signaling in Epithelial Cells

    Journal: ACS Applied Bio Materials

    doi: 10.1021/acsabm.1c00874

    Impact of CUR–PS-NPs and B-CUR on cell viability and apoptosis. Cells were exposed to the indicated concentrations of CUR–PS-NPs and B-CUR for 24 h and determined the cell viability using Alamar blue technique in (a) Huh7.5 cells and (b) A549 cells. (c) Detection of cell viability and apoptosis in treated or untreated Huh7.5 cells and A549 cells by flow cytometry using FITC Annexin V and PI staining. Treated or untreated (d) Huh7.5 cells and (e) A549 cells were also analyzed by fluorescence microscope for the detection of cell viability and apoptosis. Results are expressed as mean ± SEM of three individual experiments. “* p
    Figure Legend Snippet: Impact of CUR–PS-NPs and B-CUR on cell viability and apoptosis. Cells were exposed to the indicated concentrations of CUR–PS-NPs and B-CUR for 24 h and determined the cell viability using Alamar blue technique in (a) Huh7.5 cells and (b) A549 cells. (c) Detection of cell viability and apoptosis in treated or untreated Huh7.5 cells and A549 cells by flow cytometry using FITC Annexin V and PI staining. Treated or untreated (d) Huh7.5 cells and (e) A549 cells were also analyzed by fluorescence microscope for the detection of cell viability and apoptosis. Results are expressed as mean ± SEM of three individual experiments. “* p

    Techniques Used: Flow Cytometry, Staining, Fluorescence, Microscopy

    Effect of CUR–PS-NPs, B-CUR and PSNPs on CoV2-SP-induced IL-6 and IL-8 mediated storm in epithelial cells. Measurement of IL-6 and IL-8 protein release after 24 h exposure of 5 nM CoV2-SP to (a) Huh7.5 cells and (b) A549 cells. Quantification of IL-6 and IL-8 mRNA expression after 24 h exposure of 5 nM CoV2-SP to (c) liver epithelial Huh7.5 cells and (d) lung A549 epithelial cells. Cells were exposed to 5 nM CoV2-SP for 24 in the presence or absence of CUR–PS-NPs, B-CUR and PSNPs (5 μM). Measurement of IL-6 and IL-8 protein release by ELISA in (e) Huh7.5 cells and (f) A549 cells. Quantification of IL-6 and IL-8 mRNA by RT-qPCR in (g) Huh7.5 cells and (h) A549 cells. Results are presented as mean ± SEM of six individual experiments. (1) Unstimulated cells; (2) CoV2-SP-stimulated cells; (3) CoV2-SP-stimulated plus CUR–PS-NPs (5 μM); (4) CoV2-SP-stimulated plus B-CUR (5 μM); (5) CoV2-SP-stimulated plus PSNPs (5 μM). “# p
    Figure Legend Snippet: Effect of CUR–PS-NPs, B-CUR and PSNPs on CoV2-SP-induced IL-6 and IL-8 mediated storm in epithelial cells. Measurement of IL-6 and IL-8 protein release after 24 h exposure of 5 nM CoV2-SP to (a) Huh7.5 cells and (b) A549 cells. Quantification of IL-6 and IL-8 mRNA expression after 24 h exposure of 5 nM CoV2-SP to (c) liver epithelial Huh7.5 cells and (d) lung A549 epithelial cells. Cells were exposed to 5 nM CoV2-SP for 24 in the presence or absence of CUR–PS-NPs, B-CUR and PSNPs (5 μM). Measurement of IL-6 and IL-8 protein release by ELISA in (e) Huh7.5 cells and (f) A549 cells. Quantification of IL-6 and IL-8 mRNA by RT-qPCR in (g) Huh7.5 cells and (h) A549 cells. Results are presented as mean ± SEM of six individual experiments. (1) Unstimulated cells; (2) CoV2-SP-stimulated cells; (3) CoV2-SP-stimulated plus CUR–PS-NPs (5 μM); (4) CoV2-SP-stimulated plus B-CUR (5 μM); (5) CoV2-SP-stimulated plus PSNPs (5 μM). “# p

    Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Quantitative RT-PCR

    Impact of CUR–PS-NPs, B-CUR and PSNPs on human ACE2-CoV2-SP. (a) Concentration dependent effects of CUR–PS-NPs, B-CUR and PSNPs on interaction of ACE2 and CoV2-SP were assessed by ELISA and the results were presented as % inhibition. (b,c) Impact of 24 h treatment of different doses of CUR–PS-NPs and B-CUR on ACE2 mRNA expression in (b) Huh7.5 cells and (c) A549 cells was measured by RT-qPCR analysis. Results are presented as mean ± SEM of six individual experiments. “* p
    Figure Legend Snippet: Impact of CUR–PS-NPs, B-CUR and PSNPs on human ACE2-CoV2-SP. (a) Concentration dependent effects of CUR–PS-NPs, B-CUR and PSNPs on interaction of ACE2 and CoV2-SP were assessed by ELISA and the results were presented as % inhibition. (b,c) Impact of 24 h treatment of different doses of CUR–PS-NPs and B-CUR on ACE2 mRNA expression in (b) Huh7.5 cells and (c) A549 cells was measured by RT-qPCR analysis. Results are presented as mean ± SEM of six individual experiments. “* p

    Techniques Used: Concentration Assay, Enzyme-linked Immunosorbent Assay, Inhibition, Expressing, Quantitative RT-PCR

    Impact of CUR–PS-NPs, B-CUR and PSNPs on the release of cytokines, chemokines and growth factors by CoV2-SP-stimulated epithelial cells. (a) Profile of 37 cytokines, chemokines and growth factors in 24 h stimulation of Huh7.5 cells and A549 cells with 5 nM of CoV2-SP. Released protein levels exceeding the content of 1 pg/mL in the culture medium are presented in the graph. The results are expressed as fold change (CoV2-SP-stimulated cells vs untreated control cells). (b–j). Impacts of CUR–PS-NPs, B-CUR and PSNPs on the inflammation-related cytokines, chemokines and growth factors induced by CoV2-SP in Huh7.5 cells. (k–x) Impacts of CUR–PS-NPs, B-CUR and PSNPs on the inflammation-related cytokines, chemokines and growth induced by CoV2-SP in A549 cells. (1) Untreated and unstimulated cells; (2) CoV2-SP-stimulated cells; (3) CoV2-SP-stimulated plus CUR–PS-NPs (5 μM); (4) CoV2-SP-stimulated plus B-CUR (5 μM); (5) CoV2-SP-stimulated plus PSNPs (5 μM). Results are presented as mean ± SEM of six individual experiments. “* p
    Figure Legend Snippet: Impact of CUR–PS-NPs, B-CUR and PSNPs on the release of cytokines, chemokines and growth factors by CoV2-SP-stimulated epithelial cells. (a) Profile of 37 cytokines, chemokines and growth factors in 24 h stimulation of Huh7.5 cells and A549 cells with 5 nM of CoV2-SP. Released protein levels exceeding the content of 1 pg/mL in the culture medium are presented in the graph. The results are expressed as fold change (CoV2-SP-stimulated cells vs untreated control cells). (b–j). Impacts of CUR–PS-NPs, B-CUR and PSNPs on the inflammation-related cytokines, chemokines and growth factors induced by CoV2-SP in Huh7.5 cells. (k–x) Impacts of CUR–PS-NPs, B-CUR and PSNPs on the inflammation-related cytokines, chemokines and growth induced by CoV2-SP in A549 cells. (1) Untreated and unstimulated cells; (2) CoV2-SP-stimulated cells; (3) CoV2-SP-stimulated plus CUR–PS-NPs (5 μM); (4) CoV2-SP-stimulated plus B-CUR (5 μM); (5) CoV2-SP-stimulated plus PSNPs (5 μM). Results are presented as mean ± SEM of six individual experiments. “* p

    Techniques Used:

    11) Product Images from "RIG-I-Mediated STING Upregulation Restricts Herpes Simplex Virus 1 Infection"

    Article Title: RIG-I-Mediated STING Upregulation Restricts Herpes Simplex Virus 1 Infection

    Journal: Journal of Virology

    doi: 10.1128/JVI.00748-16

    Expression of STING is upregulated upon RIG-I signaling. A549 cells (A, B), IHHs, PC3 cells, U87 cells, Huh7.5 cells, or Huh7 cells (C), Ddx58 +/+ or Ddx58 −/− MEFs (D), and shctl- and shMAVS-transfected A549 cells (F) were uninfected or
    Figure Legend Snippet: Expression of STING is upregulated upon RIG-I signaling. A549 cells (A, B), IHHs, PC3 cells, U87 cells, Huh7.5 cells, or Huh7 cells (C), Ddx58 +/+ or Ddx58 −/− MEFs (D), and shctl- and shMAVS-transfected A549 cells (F) were uninfected or

    Techniques Used: Expressing, Transfection

    12) Product Images from "Extract from Aphloia theiformis, an edible indigenous plant from Reunion Island, impairs Zika virus attachment to the host cell surface"

    Article Title: Extract from Aphloia theiformis, an edible indigenous plant from Reunion Island, impairs Zika virus attachment to the host cell surface

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-29183-2

    A . theiformis extract exerts antiviral effect against 4 DENV clinical isolates and an epidemic Brazilian ZIKV strain. Four DENV serotypes (DENV-1, 2, 3 and 4) and a Brazilian epidemic strain of ZIKV (ZV BR2015/15261) were incubated with A . theiformis extract for 1 h at 37 °C. ( a ) Huh7.5 cells were left uninfected or were infected with DENV at an MOI of 0.1 or with ZIKV at an MOI of 0.4 for 48 h. Recombinant IFN-α 2A (200 IU.mL −1 ) was added 2 h post infection and used as positive control. The percentage of E positive cells was evaluated using the Operetta High-Content Imaging System (PerkinElmer). Results are means ± SD of three independent experiments. ( b ) The residual infectivity of treated particles was titrated in C6/36 cells using a foci-forming immunodetection assay. Data represent the means ± SD from three independent experiments. One-way ANOVA and Dunnett’s test (*p
    Figure Legend Snippet: A . theiformis extract exerts antiviral effect against 4 DENV clinical isolates and an epidemic Brazilian ZIKV strain. Four DENV serotypes (DENV-1, 2, 3 and 4) and a Brazilian epidemic strain of ZIKV (ZV BR2015/15261) were incubated with A . theiformis extract for 1 h at 37 °C. ( a ) Huh7.5 cells were left uninfected or were infected with DENV at an MOI of 0.1 or with ZIKV at an MOI of 0.4 for 48 h. Recombinant IFN-α 2A (200 IU.mL −1 ) was added 2 h post infection and used as positive control. The percentage of E positive cells was evaluated using the Operetta High-Content Imaging System (PerkinElmer). Results are means ± SD of three independent experiments. ( b ) The residual infectivity of treated particles was titrated in C6/36 cells using a foci-forming immunodetection assay. Data represent the means ± SD from three independent experiments. One-way ANOVA and Dunnett’s test (*p

    Techniques Used: Incubation, Infection, Recombinant, Positive Control, Imaging, Immunodetection

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  • 96
    ATCC huh7 5 cells
    CSMut1 design, modelling and infectivity. ( a ) The wild type E 250–270 and CSMut1 sequences are shown with mutated amino acids highlighted in red. ( b ) Wild type (on the left) and CSMut1 model (on the right) with E 250–270 in red. ( c ) Relative quantification of DV NS5 RNA in <t>Huh7.5</t> cells transfected with wild type and CSMut1 genomes at different time points. Cell associated RNA is shown in the left panel and supernatant extracted RNA in the right panel. ( d ) DV E-protein immunofluorescence staining of WT and CSMut1 120 hours after genome transfection in Huh7.5 cells (bars correspond to 32 μM).
    Huh7 5 Cells, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    96
    ATCC human hepatocellular carcinoma cell lines huh7
    Replication efficiency of vaccinia virus strain GLV-1h68 in <t>HuH7</t> (A) and PLC (B) cells at an MOI of 0.1. Supernatants were collected from virus-infected cells at various time points (hours) post-infection (hpi). Viral titers were determined as pfu per well in triplicates. Averages plus standard deviation are plotted.
    Human Hepatocellular Carcinoma Cell Lines Huh7, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    CSMut1 design, modelling and infectivity. ( a ) The wild type E 250–270 and CSMut1 sequences are shown with mutated amino acids highlighted in red. ( b ) Wild type (on the left) and CSMut1 model (on the right) with E 250–270 in red. ( c ) Relative quantification of DV NS5 RNA in Huh7.5 cells transfected with wild type and CSMut1 genomes at different time points. Cell associated RNA is shown in the left panel and supernatant extracted RNA in the right panel. ( d ) DV E-protein immunofluorescence staining of WT and CSMut1 120 hours after genome transfection in Huh7.5 cells (bars correspond to 32 μM).

    Journal: Scientific Reports

    Article Title: Genome-wide analyses reveal a highly conserved Dengue virus envelope peptide which is critical for virus viability and antigenic in humans

    doi: 10.1038/srep36339

    Figure Lengend Snippet: CSMut1 design, modelling and infectivity. ( a ) The wild type E 250–270 and CSMut1 sequences are shown with mutated amino acids highlighted in red. ( b ) Wild type (on the left) and CSMut1 model (on the right) with E 250–270 in red. ( c ) Relative quantification of DV NS5 RNA in Huh7.5 cells transfected with wild type and CSMut1 genomes at different time points. Cell associated RNA is shown in the left panel and supernatant extracted RNA in the right panel. ( d ) DV E-protein immunofluorescence staining of WT and CSMut1 120 hours after genome transfection in Huh7.5 cells (bars correspond to 32 μM).

    Article Snippet: Briefly, Huh7.5 cells were transfected with wild type or CSMut1 RNA using Lipofectin, fixed after 120 hours, and stained with monoclonal anti-E antibody (4G2 - ATCC® HB-112™ ), using Alexa Fluor 488 rabbit anti-mouse IgG (H + L, Life Technologies) as a secondary antibody, and DAPI counter stain (Molecular Probes).

    Techniques: Infection, Transfection, Immunofluorescence, Staining

    IL-17A upregulates the production of pro-angiogenic CXC chemokines in liver cancer cells. The effect of IL-17A overexpression on the expression levels of angiogenic factors in (A) Huh7.5 and (B) HepG2 cells was determined by RT-qPCR. *P

    Journal: Molecular Medicine Reports

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    doi: 10.3892/mmr.2019.10310

    Figure Lengend Snippet: IL-17A upregulates the production of pro-angiogenic CXC chemokines in liver cancer cells. The effect of IL-17A overexpression on the expression levels of angiogenic factors in (A) Huh7.5 and (B) HepG2 cells was determined by RT-qPCR. *P

    Article Snippet: Cell cultures The liver cancer cell line HepG2 ( , ) was supplied by American Type Culture Collection and Huh7.5 ( ) cells were gifted by Dr. Aihua Zheng (Chinese Academy of Sciences).

    Techniques: Over Expression, Expressing, Quantitative RT-PCR

    Expression of IL17RA and VEGFR2 in liver cancer-derived cell lines. The expression of IL17RA and VEGFR2 in HepG2 and Huh7.5 cells was examined by reverse transcription-quantitative PCR. GAPDH served as the internal control. **P

    Journal: Molecular Medicine Reports

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    doi: 10.3892/mmr.2019.10310

    Figure Lengend Snippet: Expression of IL17RA and VEGFR2 in liver cancer-derived cell lines. The expression of IL17RA and VEGFR2 in HepG2 and Huh7.5 cells was examined by reverse transcription-quantitative PCR. GAPDH served as the internal control. **P

    Article Snippet: Cell cultures The liver cancer cell line HepG2 ( , ) was supplied by American Type Culture Collection and Huh7.5 ( ) cells were gifted by Dr. Aihua Zheng (Chinese Academy of Sciences).

    Techniques: Expressing, Derivative Assay, Real-time Polymerase Chain Reaction

    IL-17A has no effect on the proliferation of liver cancer cells. (A) HepG2 and Huh7.5 cells overexpressing EGFP or IL-17A were cultured in 6-well plates for 24 h. The concentration of IL-17A in the cell-free supernatants was measured by IL-17A ELISA. **P

    Journal: Molecular Medicine Reports

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    doi: 10.3892/mmr.2019.10310

    Figure Lengend Snippet: IL-17A has no effect on the proliferation of liver cancer cells. (A) HepG2 and Huh7.5 cells overexpressing EGFP or IL-17A were cultured in 6-well plates for 24 h. The concentration of IL-17A in the cell-free supernatants was measured by IL-17A ELISA. **P

    Article Snippet: Cell cultures The liver cancer cell line HepG2 ( , ) was supplied by American Type Culture Collection and Huh7.5 ( ) cells were gifted by Dr. Aihua Zheng (Chinese Academy of Sciences).

    Techniques: Cell Culture, Concentration Assay, Enzyme-linked Immunosorbent Assay

    Effect of IL-17A on liver cancer cell-induced endothelial cell chemotaxis. The chemotaxis effect of the supernatants from liver cancer cells on HUVEC invasion was examined by Transwell assays. The effect of IL-17A overexpression in (A and C) Huh7.5 or (B and D) HepG2 cells on endothelial cell chemotaxis. Antibody against IL17RA (5 µg/ml) was added during liver cancer cell culture. Chemokine (C-X-C motif) receptor 2 inhibitor SB225002 was added to the supernatants from Huh7.5-EGFP or Huh7.5-IL17A. (A, B and E) Representative 4′,6-diamidino-2-phenylindole staining images of migrated HUVEC are presented and (C, D and F) the calculated values are shown. Data were derived from three independent experiments. Five randomly selected images (magnification, ×400) were used in the calculation for each well. *P

    Journal: Molecular Medicine Reports

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    doi: 10.3892/mmr.2019.10310

    Figure Lengend Snippet: Effect of IL-17A on liver cancer cell-induced endothelial cell chemotaxis. The chemotaxis effect of the supernatants from liver cancer cells on HUVEC invasion was examined by Transwell assays. The effect of IL-17A overexpression in (A and C) Huh7.5 or (B and D) HepG2 cells on endothelial cell chemotaxis. Antibody against IL17RA (5 µg/ml) was added during liver cancer cell culture. Chemokine (C-X-C motif) receptor 2 inhibitor SB225002 was added to the supernatants from Huh7.5-EGFP or Huh7.5-IL17A. (A, B and E) Representative 4′,6-diamidino-2-phenylindole staining images of migrated HUVEC are presented and (C, D and F) the calculated values are shown. Data were derived from three independent experiments. Five randomly selected images (magnification, ×400) were used in the calculation for each well. *P

    Article Snippet: Cell cultures The liver cancer cell line HepG2 ( , ) was supplied by American Type Culture Collection and Huh7.5 ( ) cells were gifted by Dr. Aihua Zheng (Chinese Academy of Sciences).

    Techniques: Chemotaxis Assay, Over Expression, Cell Culture, Staining, Derivative Assay

    Overexpression of IL-17A promotes Huh7.5 tumor growth in vivo . Representative tumors from a (A and B) subcutaneous model (n=6) and (C and D) liver model (n=5) are presented; (A and C) Huh7.5-EGFP and (Band D) Huh7.5-IL17A. Scale bar, 5 mm. (E) The tumor volumes of Huh7.5-EGFP and Huh7.5-IL17A tumors in the subcutaneous model were measured at the time-points indicated, and (F) the tumor weights are shown. Data are presented as the mean ± SD. **P

    Journal: Molecular Medicine Reports

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    doi: 10.3892/mmr.2019.10310

    Figure Lengend Snippet: Overexpression of IL-17A promotes Huh7.5 tumor growth in vivo . Representative tumors from a (A and B) subcutaneous model (n=6) and (C and D) liver model (n=5) are presented; (A and C) Huh7.5-EGFP and (Band D) Huh7.5-IL17A. Scale bar, 5 mm. (E) The tumor volumes of Huh7.5-EGFP and Huh7.5-IL17A tumors in the subcutaneous model were measured at the time-points indicated, and (F) the tumor weights are shown. Data are presented as the mean ± SD. **P

    Article Snippet: Cell cultures The liver cancer cell line HepG2 ( , ) was supplied by American Type Culture Collection and Huh7.5 ( ) cells were gifted by Dr. Aihua Zheng (Chinese Academy of Sciences).

    Techniques: Over Expression, In Vivo

    Overexpression of IL-17A promotes growth and angiogenesis in Huh7.5 orthotopic tumors. The morphology of Huh7.5-EGFP- or Huh7.5-IL17A-derived liver tumors was examined by (A and B) hematoxylin and eosin staining, and (C and D) the blood vessels were observed via CD31 immunohistochemistry. Scale bar, 50 µm. (E) Quantitative analysis of the immunostaining-positive area in C D. Data are presented as the mean ± SD. **P

    Journal: Molecular Medicine Reports

    Article Title: IL-17A promotes CXCR2-dependent angiogenesis in a mouse model of liver cancer

    doi: 10.3892/mmr.2019.10310

    Figure Lengend Snippet: Overexpression of IL-17A promotes growth and angiogenesis in Huh7.5 orthotopic tumors. The morphology of Huh7.5-EGFP- or Huh7.5-IL17A-derived liver tumors was examined by (A and B) hematoxylin and eosin staining, and (C and D) the blood vessels were observed via CD31 immunohistochemistry. Scale bar, 50 µm. (E) Quantitative analysis of the immunostaining-positive area in C D. Data are presented as the mean ± SD. **P

    Article Snippet: Cell cultures The liver cancer cell line HepG2 ( , ) was supplied by American Type Culture Collection and Huh7.5 ( ) cells were gifted by Dr. Aihua Zheng (Chinese Academy of Sciences).

    Techniques: Over Expression, Derivative Assay, Staining, Immunohistochemistry, Immunostaining

    NSAID treatment does not affect SARS-CoV-2 entry or replication (A-B) Calu-3 (A) and Huh7.5 (B) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with SARS2-VSVpp or G-VSVpp expressing Renilla luciferase. Luminescence was measured at 24 hours post infection (hpi) and normalized to DMSO for each infection. (C-D) Calu-3 (C) and Huh7.5 (D) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with mNeonGreen reporter replication-competent SARS-CoV-2 (icSARS-CoV-2-mNG) at a MOI of 1. Frequency of infected cells was measured by mNeonGreen expression at 1, 2, and 3 dpi. All data points in this figure are presented as mean ± SEM. Data were analyzed by Student’s two-tailed, unpaired t -test (A-B) and two-way ANOVA (C-D). ns, not significant. Data in (A-B) are representative of two independent experiments with four replicates per condition. Data in (C-D) are representative of two independent experiments with five replicates per condition.

    Journal: bioRxiv

    Article Title: Cyclooxgenase-2 is induced by SARS-CoV-2 infection but does not affect viral entry or replication

    doi: 10.1101/2020.09.24.312769

    Figure Lengend Snippet: NSAID treatment does not affect SARS-CoV-2 entry or replication (A-B) Calu-3 (A) and Huh7.5 (B) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with SARS2-VSVpp or G-VSVpp expressing Renilla luciferase. Luminescence was measured at 24 hours post infection (hpi) and normalized to DMSO for each infection. (C-D) Calu-3 (C) and Huh7.5 (D) cells were pre-treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours and then infected with mNeonGreen reporter replication-competent SARS-CoV-2 (icSARS-CoV-2-mNG) at a MOI of 1. Frequency of infected cells was measured by mNeonGreen expression at 1, 2, and 3 dpi. All data points in this figure are presented as mean ± SEM. Data were analyzed by Student’s two-tailed, unpaired t -test (A-B) and two-way ANOVA (C-D). ns, not significant. Data in (A-B) are representative of two independent experiments with four replicates per condition. Data in (C-D) are representative of two independent experiments with five replicates per condition.

    Article Snippet: Generation of SARS-CoV-2 stocks As previously described , SARS-CoV-2 P1 stock was generated by inoculating Huh7.5 cells with SARS-CoV-2 isolate USA-WA1/2020 (BEI Resources, NR-52281) at a MOI of 0.01 for three days.

    Techniques: Infection, Expressing, Luciferase, Two Tailed Test

    SARS-CoV-2 infection induces PTGS2 expression in human and mouse systems (A) Calu-3 cells were infected with SARS-CoV-2 at a multiplicity of infection (MOI) of 0.05. PTGS2 expression was measured at 2 days post infection (dpi), normalized to ACTB . (B-C) PTGS2 expression in Calu-3 (B) and ACE2-overexpressing A549 (A549-ACE2) (C) cells following SARS-CoV-2 infection. Data are from GSE147507 (Blanco-Melo et al., 2020). (D) Huh7.5 cells were infected with SARS-CoV-2 at a MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (E) Human bronchial epithelial cells (HBECs) were cultured at an air-liquid interface and then infected at the apical surface with 10 4 plaque-forming units (PFU) of SARS-CoV-2. Cells were collected at 1, 2, and 3 dpi for single-cell RNA sequencing (scRNA-seq) ( 16 ). Volcano plot of differentially expressed genes in infected versus bystander ciliated cells pooled from all time points. PTGS2 is highlighted. (F) K18-hACE2 mice were infected intranasally with 1.2 × 10 6 PFU of SARS-CoV-2. Ptgs2 expression in the lung was measured at 0, 2, 4, and 7 dpi. (G) Ptgs2 expression in the lung of K18-hACE2 mice following intranasal SARS-CoV-2 infection. Data are from GSE154104 (Winkler et al., 2020). All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (A, D, F); Student’s two-tailed, unpaired t -test (B, C, G); and two-sided Mann-Whitney U test with continuity and Benjamini-Hochberg correction (E). *P

    Journal: bioRxiv

    Article Title: Cyclooxgenase-2 is induced by SARS-CoV-2 infection but does not affect viral entry or replication

    doi: 10.1101/2020.09.24.312769

    Figure Lengend Snippet: SARS-CoV-2 infection induces PTGS2 expression in human and mouse systems (A) Calu-3 cells were infected with SARS-CoV-2 at a multiplicity of infection (MOI) of 0.05. PTGS2 expression was measured at 2 days post infection (dpi), normalized to ACTB . (B-C) PTGS2 expression in Calu-3 (B) and ACE2-overexpressing A549 (A549-ACE2) (C) cells following SARS-CoV-2 infection. Data are from GSE147507 (Blanco-Melo et al., 2020). (D) Huh7.5 cells were infected with SARS-CoV-2 at a MOI of 0.05. PTGS2 expression was measured at 2 dpi, normalized to ACTB . (E) Human bronchial epithelial cells (HBECs) were cultured at an air-liquid interface and then infected at the apical surface with 10 4 plaque-forming units (PFU) of SARS-CoV-2. Cells were collected at 1, 2, and 3 dpi for single-cell RNA sequencing (scRNA-seq) ( 16 ). Volcano plot of differentially expressed genes in infected versus bystander ciliated cells pooled from all time points. PTGS2 is highlighted. (F) K18-hACE2 mice were infected intranasally with 1.2 × 10 6 PFU of SARS-CoV-2. Ptgs2 expression in the lung was measured at 0, 2, 4, and 7 dpi. (G) Ptgs2 expression in the lung of K18-hACE2 mice following intranasal SARS-CoV-2 infection. Data are from GSE154104 (Winkler et al., 2020). All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (A, D, F); Student’s two-tailed, unpaired t -test (B, C, G); and two-sided Mann-Whitney U test with continuity and Benjamini-Hochberg correction (E). *P

    Article Snippet: Generation of SARS-CoV-2 stocks As previously described , SARS-CoV-2 P1 stock was generated by inoculating Huh7.5 cells with SARS-CoV-2 isolate USA-WA1/2020 (BEI Resources, NR-52281) at a MOI of 0.01 for three days.

    Techniques: Infection, Expressing, Cell Culture, RNA Sequencing Assay, Mouse Assay, Two Tailed Test, MANN-WHITNEY

    NSAID treatment does not affect ACE2 expression in human cell lines (A-B) Calu-3 (A) and Huh7.5 (B) cells were treated with different concentrations of ibuprofen or meloxicam for 48 hours. Cell viability was measured and calculated as a percentage of no treatment. (C) Calu-3 cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 48 hours. Levels of prostaglandin E 2 (PGE 2 ) were measured in the supernatant. Dotted line represents limit of detection. (D-E) Calu-3 (D) and Huh7.5 (E) cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours. ACE2 expression was measured and normalized to ACTB . All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (C-E). **P

    Journal: bioRxiv

    Article Title: Cyclooxgenase-2 is induced by SARS-CoV-2 infection but does not affect viral entry or replication

    doi: 10.1101/2020.09.24.312769

    Figure Lengend Snippet: NSAID treatment does not affect ACE2 expression in human cell lines (A-B) Calu-3 (A) and Huh7.5 (B) cells were treated with different concentrations of ibuprofen or meloxicam for 48 hours. Cell viability was measured and calculated as a percentage of no treatment. (C) Calu-3 cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 48 hours. Levels of prostaglandin E 2 (PGE 2 ) were measured in the supernatant. Dotted line represents limit of detection. (D-E) Calu-3 (D) and Huh7.5 (E) cells were treated with DMSO, 50 μM ibuprofen, or 50 μM meloxicam for 24 hours. ACE2 expression was measured and normalized to ACTB . All data points in this figure are presented as mean ± SEM. Data were analyzed by Welch’s two-tailed, unpaired t -test (C-E). **P

    Article Snippet: Generation of SARS-CoV-2 stocks As previously described , SARS-CoV-2 P1 stock was generated by inoculating Huh7.5 cells with SARS-CoV-2 isolate USA-WA1/2020 (BEI Resources, NR-52281) at a MOI of 0.01 for three days.

    Techniques: Expressing, Two Tailed Test

    Replication efficiency of vaccinia virus strain GLV-1h68 in HuH7 (A) and PLC (B) cells at an MOI of 0.1. Supernatants were collected from virus-infected cells at various time points (hours) post-infection (hpi). Viral titers were determined as pfu per well in triplicates. Averages plus standard deviation are plotted.

    Journal: PLoS ONE

    Article Title: Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68

    doi: 10.1371/journal.pone.0022069

    Figure Lengend Snippet: Replication efficiency of vaccinia virus strain GLV-1h68 in HuH7 (A) and PLC (B) cells at an MOI of 0.1. Supernatants were collected from virus-infected cells at various time points (hours) post-infection (hpi). Viral titers were determined as pfu per well in triplicates. Averages plus standard deviation are plotted.

    Article Snippet: Cell lines African green monkey kidney fibroblasts (CV-1, American Type Culture Collection, ATCC-No. CCL-70) and two human hepatocellular carcinoma cell lines HuH7 (ATCC CCL-185) and PLC/PRF/5 (PLC; ATCC CRL 8024) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with antibiotics (100 units/ml penicillin G, 100 units/ml streptomycin) and 10% fetal bovine serum (FBS; Invitrogen GmbH, Karlsruhe, Germany) at 37°C under 5% CO2 .

    Techniques: Planar Chromatography, Infection, Standard Deviation

    Immunohistochemical staining of MHC class II-positive cells in GLV-1h68-infected and uninfected HuH7 or PLC xenograft tumors at 10 dpi. Mice bearing tumors of HuH7 (A, B) or PLC (C, D) origin either were mock treated (A, C) or infected with GLV-1h68 (B, D). Tumor sections were labeled with an anti-MHCII antibody (red) and viral infection was indicated by GFP fluorescence (green). In addition, overlays of MHCII and GFP signals and transmission images (bright-field) are shown. Scale bars represent 1 mm.

    Journal: PLoS ONE

    Article Title: Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68

    doi: 10.1371/journal.pone.0022069

    Figure Lengend Snippet: Immunohistochemical staining of MHC class II-positive cells in GLV-1h68-infected and uninfected HuH7 or PLC xenograft tumors at 10 dpi. Mice bearing tumors of HuH7 (A, B) or PLC (C, D) origin either were mock treated (A, C) or infected with GLV-1h68 (B, D). Tumor sections were labeled with an anti-MHCII antibody (red) and viral infection was indicated by GFP fluorescence (green). In addition, overlays of MHCII and GFP signals and transmission images (bright-field) are shown. Scale bars represent 1 mm.

    Article Snippet: Cell lines African green monkey kidney fibroblasts (CV-1, American Type Culture Collection, ATCC-No. CCL-70) and two human hepatocellular carcinoma cell lines HuH7 (ATCC CCL-185) and PLC/PRF/5 (PLC; ATCC CRL 8024) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with antibiotics (100 units/ml penicillin G, 100 units/ml streptomycin) and 10% fetal bovine serum (FBS; Invitrogen GmbH, Karlsruhe, Germany) at 37°C under 5% CO2 .

    Techniques: Immunohistochemistry, Staining, Infection, Planar Chromatography, Mouse Assay, Labeling, Fluorescence, Transmission Assay

    Analysis of GLV-1h68 virus-induced changes in HuH7- or PLC-tumor vascularization by confocal laser microscopy. Determination of vascular density using CD31 immunohistochemistry in virus- treated and non-treated HuH7 or PLC, tumors (A). The vascular density was measured in CD31-labeled tumor cross-sections (n = 6 per group) and presented as mean values +/− standard deviations. The asterisks (**) indicate a significant difference between experimental groups (** P

    Journal: PLoS ONE

    Article Title: Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68

    doi: 10.1371/journal.pone.0022069

    Figure Lengend Snippet: Analysis of GLV-1h68 virus-induced changes in HuH7- or PLC-tumor vascularization by confocal laser microscopy. Determination of vascular density using CD31 immunohistochemistry in virus- treated and non-treated HuH7 or PLC, tumors (A). The vascular density was measured in CD31-labeled tumor cross-sections (n = 6 per group) and presented as mean values +/− standard deviations. The asterisks (**) indicate a significant difference between experimental groups (** P

    Article Snippet: Cell lines African green monkey kidney fibroblasts (CV-1, American Type Culture Collection, ATCC-No. CCL-70) and two human hepatocellular carcinoma cell lines HuH7 (ATCC CCL-185) and PLC/PRF/5 (PLC; ATCC CRL 8024) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with antibiotics (100 units/ml penicillin G, 100 units/ml streptomycin) and 10% fetal bovine serum (FBS; Invitrogen GmbH, Karlsruhe, Germany) at 37°C under 5% CO2 .

    Techniques: Planar Chromatography, Microscopy, Immunohistochemistry, Labeling

    Growth of HuH7 and PLC tumors in GLV-1h68- and mock-treated mice. Groups of HuH7 ( Fig. 5A ) or PLC tumor-bearing nude mice ( Fig. 5B ) were either treated with a single dose of 5×10 6 pfu GLV-1h68 (n = 5) or with PBS (mock control, n = 5). Tumor size was measured twice a week. Two-way analysis of variance (2way ANOVA) with Bonferroni post-test was used for comparison of two corresponding data points between groups. P

    Journal: PLoS ONE

    Article Title: Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68

    doi: 10.1371/journal.pone.0022069

    Figure Lengend Snippet: Growth of HuH7 and PLC tumors in GLV-1h68- and mock-treated mice. Groups of HuH7 ( Fig. 5A ) or PLC tumor-bearing nude mice ( Fig. 5B ) were either treated with a single dose of 5×10 6 pfu GLV-1h68 (n = 5) or with PBS (mock control, n = 5). Tumor size was measured twice a week. Two-way analysis of variance (2way ANOVA) with Bonferroni post-test was used for comparison of two corresponding data points between groups. P

    Article Snippet: Cell lines African green monkey kidney fibroblasts (CV-1, American Type Culture Collection, ATCC-No. CCL-70) and two human hepatocellular carcinoma cell lines HuH7 (ATCC CCL-185) and PLC/PRF/5 (PLC; ATCC CRL 8024) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with antibiotics (100 units/ml penicillin G, 100 units/ml streptomycin) and 10% fetal bovine serum (FBS; Invitrogen GmbH, Karlsruhe, Germany) at 37°C under 5% CO2 .

    Techniques: Planar Chromatography, Mouse Assay

    Viability of hepatocellular carcinoma HuH7 (A) and PLC (B) cells after GLV-1h68 infection at MOIs of 0.1 and 1.0, respectively. Viable cells after infection with GLV-1h68 were determined by use of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) (Sigma, Taufkirchen, Germany). Mean values (n = 3) and standard deviations are shown as percentages of respective controls.

    Journal: PLoS ONE

    Article Title: Efficient Colonization and Therapy of Human Hepatocellular Carcinoma (HCC) Using the Oncolytic Vaccinia Virus Strain GLV-1h68

    doi: 10.1371/journal.pone.0022069

    Figure Lengend Snippet: Viability of hepatocellular carcinoma HuH7 (A) and PLC (B) cells after GLV-1h68 infection at MOIs of 0.1 and 1.0, respectively. Viable cells after infection with GLV-1h68 were determined by use of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) (Sigma, Taufkirchen, Germany). Mean values (n = 3) and standard deviations are shown as percentages of respective controls.

    Article Snippet: Cell lines African green monkey kidney fibroblasts (CV-1, American Type Culture Collection, ATCC-No. CCL-70) and two human hepatocellular carcinoma cell lines HuH7 (ATCC CCL-185) and PLC/PRF/5 (PLC; ATCC CRL 8024) were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with antibiotics (100 units/ml penicillin G, 100 units/ml streptomycin) and 10% fetal bovine serum (FBS; Invitrogen GmbH, Karlsruhe, Germany) at 37°C under 5% CO2 .

    Techniques: Planar Chromatography, Infection, MTT Assay