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cell lines 369 primary human pulmonary microvascular endothelial cells hpmec  (PromoCell)


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    PromoCell cell lines 369 primary human pulmonary microvascular endothelial cells hpmec
    Cell Lines 369 Primary Human Pulmonary Microvascular Endothelial Cells Hpmec, supplied by PromoCell, used in various techniques. Bioz Stars score: 96/100, based on 159 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/human+primary+cells/pm42262358-129-10-20?v=PromoCell
    Average 96 stars, based on 159 article reviews
    cell lines 369 primary human pulmonary microvascular endothelial cells hpmec - by Bioz Stars, 2026-07
    96/100 stars

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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for <t>epithelial</t> damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)
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    Assembly and characterization of human 3D liver spheroids via DNA origami NAC-linkers. (A) Schematic of 3D liver spheroid self-assembly from primary human <t>hepatocytes,</t> liver sinusoidal endothelial cells, and Kupffer cells using NAC-linkers. (B) Atomic force microscopy image of NAC-linkers. Scale bars, 200 nm. (C) 1% agarose gel electrophoresis confirming cholesterol-modified NAC-linkers assembly (lanes: DNA marker, M13mp18 scaffold, and NAC-linkers). (D) Bright-field image of a mature spheroid. (E) Hematoxylin and eosin (H&E) staining of a spheroid section. (F) Immunofluorescence staining of cell type markers in human 3D liver spheroids: albumin (ALB, hepatocytes), CD31 (endothelial cells), and CD68 (Kupffer cells). Scale bars, 200 μm.
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    Image Search Results


    Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for epithelial damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Journal: The Cell Surface

    Article Title: Compromising UPD-sugar nucleotide biosynthesis attenuates Candida albicans viability, virulence and drug sensitivity

    doi: 10.1016/j.tcsw.2026.100170

    Figure Lengend Snippet: Host cell damage and virulence capacity of mutants in sugar nucleotide biosynthesis. (A) Mutants grown in +/− 25 μg/ml Dox screened for epithelial damage using A-431 cells by LDH assay. The mean LDH released at 24 h post co-incubation is shown for repressed mutants (grown in presence of Dox; blue bars) and No-Dox controls (red bars). Red and blue horizontal lines indicate the mean LDH activity for wild type control (No-Dox) and wild type grown in presence of Dox respectively. Welsh t-test used for statistical analysis; error bars represent standard error of mean; p**** < 0.0001. (B) Survival plots of G. mellonella larvae infected with C. albicans mutants in: (I) GDP-mannose, (II) UDP-glucose and (III) UDP- N -acetylglucosamine biosynthesis in presence (solid lines) and absence (dotted lines) of Dox. No killing or improved survival was observed for a number of repressed mutants. No killing was observed in control larvae injected with equivalent volume of PBS. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)

    Article Snippet: Human epithelial cells derived from a vulvar squamous cell carcinoma (A-431 cell line; ATCC No.: CRL-1555) were cultured and maintained in DMEM medium supplemented with 10% ( v /v) heat inactivated foetal calf serum, 5% penicillin and 5% streptomycin.

    Techniques: Lactate Dehydrogenase Assay, Incubation, Activity Assay, Control, Infection, Injection

    Assembly and characterization of human 3D liver spheroids via DNA origami NAC-linkers. (A) Schematic of 3D liver spheroid self-assembly from primary human hepatocytes, liver sinusoidal endothelial cells, and Kupffer cells using NAC-linkers. (B) Atomic force microscopy image of NAC-linkers. Scale bars, 200 nm. (C) 1% agarose gel electrophoresis confirming cholesterol-modified NAC-linkers assembly (lanes: DNA marker, M13mp18 scaffold, and NAC-linkers). (D) Bright-field image of a mature spheroid. (E) Hematoxylin and eosin (H&E) staining of a spheroid section. (F) Immunofluorescence staining of cell type markers in human 3D liver spheroids: albumin (ALB, hepatocytes), CD31 (endothelial cells), and CD68 (Kupffer cells). Scale bars, 200 μm.

    Journal: One Health

    Article Title: Human 3D liver spheroids support productive infection of a novel tick-borne phenuivirus

    doi: 10.1016/j.onehlt.2026.101321

    Figure Lengend Snippet: Assembly and characterization of human 3D liver spheroids via DNA origami NAC-linkers. (A) Schematic of 3D liver spheroid self-assembly from primary human hepatocytes, liver sinusoidal endothelial cells, and Kupffer cells using NAC-linkers. (B) Atomic force microscopy image of NAC-linkers. Scale bars, 200 nm. (C) 1% agarose gel electrophoresis confirming cholesterol-modified NAC-linkers assembly (lanes: DNA marker, M13mp18 scaffold, and NAC-linkers). (D) Bright-field image of a mature spheroid. (E) Hematoxylin and eosin (H&E) staining of a spheroid section. (F) Immunofluorescence staining of cell type markers in human 3D liver spheroids: albumin (ALB, hepatocytes), CD31 (endothelial cells), and CD68 (Kupffer cells). Scale bars, 200 μm.

    Article Snippet: Primary human hepatocytes, liver sinusoidal endothelial cells, and Kupffer cells (IxCell Biotechnology) were mixed at specific ratios and co-incubated with NAC-Linker A and B (Puheng Biomedicine, NAC001) to facilitate NAC structure formation on the cell surfaces.

    Techniques: Microscopy, Agarose Gel Electrophoresis, Modification, Marker, Staining, Immunofluorescence

    Adaptation and pathogenesis of MKWV in human 3D liver spheroids. (A) Schematic of serial passaging of the HLJ1 strain in spheroids, yielding the adapted NAC-Org5 strain. (B, C) Viral RNA copies (B) and TCID₅₀ titers (C) across passages (P1-P5). (D) Bright-field image of spheroids infected with passage 5 (P5) virus, showing structural disruption. Scale bar, 100 μm. (E) Quantification of spheroid diameter post-infection. (F) Transmission electron micrographs of virions within cytoplasmic vesicles of infected spheroids. Scale bars: 1 μm (left), 200 nm (right). (G) Representative images and quantification of nuclei showing infection-induced cell death. Scale bar, 200 μm. (H) Western blot detecting cleaved caspase-3 in spheroids at 48 and 72 h post-infection (hpi). (I) Multiplex immunofluorescence showing NAC-Org5 tropism for CD31 + endothelial cells and CD68 + Kupffer cells, with weaker detection in ALB + hepatocytes. Scale bar, 200 μm. (J) Functional assessment of infected spheroids: ATP (viability), ALT/AST/LDH (damage), ALB/urea (synthetic function). (K) RT-qPCR analysis of pro-inflammatory cytokine mRNA expression, normalized to β-actin. Data are mean ± SD ( n = 5 biological replicates). * p < 0.05, ** p < 0.01.

    Journal: One Health

    Article Title: Human 3D liver spheroids support productive infection of a novel tick-borne phenuivirus

    doi: 10.1016/j.onehlt.2026.101321

    Figure Lengend Snippet: Adaptation and pathogenesis of MKWV in human 3D liver spheroids. (A) Schematic of serial passaging of the HLJ1 strain in spheroids, yielding the adapted NAC-Org5 strain. (B, C) Viral RNA copies (B) and TCID₅₀ titers (C) across passages (P1-P5). (D) Bright-field image of spheroids infected with passage 5 (P5) virus, showing structural disruption. Scale bar, 100 μm. (E) Quantification of spheroid diameter post-infection. (F) Transmission electron micrographs of virions within cytoplasmic vesicles of infected spheroids. Scale bars: 1 μm (left), 200 nm (right). (G) Representative images and quantification of nuclei showing infection-induced cell death. Scale bar, 200 μm. (H) Western blot detecting cleaved caspase-3 in spheroids at 48 and 72 h post-infection (hpi). (I) Multiplex immunofluorescence showing NAC-Org5 tropism for CD31 + endothelial cells and CD68 + Kupffer cells, with weaker detection in ALB + hepatocytes. Scale bar, 200 μm. (J) Functional assessment of infected spheroids: ATP (viability), ALT/AST/LDH (damage), ALB/urea (synthetic function). (K) RT-qPCR analysis of pro-inflammatory cytokine mRNA expression, normalized to β-actin. Data are mean ± SD ( n = 5 biological replicates). * p < 0.05, ** p < 0.01.

    Article Snippet: Primary human hepatocytes, liver sinusoidal endothelial cells, and Kupffer cells (IxCell Biotechnology) were mixed at specific ratios and co-incubated with NAC-Linker A and B (Puheng Biomedicine, NAC001) to facilitate NAC structure formation on the cell surfaces.

    Techniques: Passaging, Infection, Virus, Disruption, Transmission Assay, Western Blot, Multiplex Assay, Immunofluorescence, Functional Assay, Quantitative RT-PCR, Expressing

    Pathogenicity of the NAC-Org5 strain in murine models. (A) Experimental schematic for intracranial (3-day-old) and intraperitoneal (3-week-old) inoculation of BALB/c mice. (B, C) Survival (B) and weight change (C) of suckling mice after NAC-Org5 infection. (D) Viral load in tissues and blood of suckling mice at 7 dpi. (E, F) Survival (E) and weight change (F) of 3-week-old mice. (G) Viral load in tissues and blood of 3-week-old mice at 7 dpi. Data are from 3 independent experiments. (H) Representative H& E -stained liver sections from 3-week-old mice at 7 and 15 dpi, showing inflammatory infiltrates and hepatocyte necrosis that resolves by 15 dpi. Scale bar, 100 μm. *** p < 0.001.

    Journal: One Health

    Article Title: Human 3D liver spheroids support productive infection of a novel tick-borne phenuivirus

    doi: 10.1016/j.onehlt.2026.101321

    Figure Lengend Snippet: Pathogenicity of the NAC-Org5 strain in murine models. (A) Experimental schematic for intracranial (3-day-old) and intraperitoneal (3-week-old) inoculation of BALB/c mice. (B, C) Survival (B) and weight change (C) of suckling mice after NAC-Org5 infection. (D) Viral load in tissues and blood of suckling mice at 7 dpi. (E, F) Survival (E) and weight change (F) of 3-week-old mice. (G) Viral load in tissues and blood of 3-week-old mice at 7 dpi. Data are from 3 independent experiments. (H) Representative H& E -stained liver sections from 3-week-old mice at 7 and 15 dpi, showing inflammatory infiltrates and hepatocyte necrosis that resolves by 15 dpi. Scale bar, 100 μm. *** p < 0.001.

    Article Snippet: Primary human hepatocytes, liver sinusoidal endothelial cells, and Kupffer cells (IxCell Biotechnology) were mixed at specific ratios and co-incubated with NAC-Linker A and B (Puheng Biomedicine, NAC001) to facilitate NAC structure formation on the cell surfaces.

    Techniques: Infection, Staining