primary human umbilical vein endothelial cells  (PromoCell)

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

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

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

Journal: Materials Today Bio

Article Title: Injectable chitosan-based hydrogel via in situ gelation modulates the inflammatory microenvironment and facilitates minimally invasive repair of peripheral nerve injury

doi: 10.1016/j.mtbio.2026.102814

Figure Lengend Snippet: Pro-angiogenic and pro-migratory effects of hydrogels. Immunofluorescence staining shows blood vessel formation of HUVECs in LPS-macrophage condition medium (A). Scratch assays and Transwell migration assays of HUVECs (B) and L929 cells (C). Quantification of junctions (D), branches (E), wound closure percentage (F–G) and migrated cells (H–I). One-way ANOVA with Tukey's post hoc test and n = 3 for D-I; ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001, n.s. ANOVA, analysis of variance; CS, chitosan; IBU, ibuprofen; GP, genipin; MA, methacrylic anhydride; LPS, lipopolysaccharides; HUVEC, human umbilical vein endothelial cell; n.s., not significant.

Article Snippet: Mouse fibroblasts (L929, ATCC), human umbilical vein endothelial cells (HUVECs, ATCC), and mouse macrophages (RAW 264.7, ATCC) were provided by the Cell Bank of the Chinese Academy of Sciences.

Techniques: Immunofluorescence, Staining, Migration

Journal: Regenerative Therapy

Article Title: Airway basal stem cell derived extracellular vesicles promote lung repair in chronic obstructive pulmonary disease

doi: 10.1016/j.reth.2026.101068

Figure Lengend Snippet: Characterization of BC-EVs. (a) Representative transmission electron microscopy image of BC-EVs. Scale bar, 100 nm. (b) Size distribution of BC-EVs determined by Nano-Flow Cytometry. (c) Western blotting analysis showing the expression of EV markers TSG101 and CD63, and the negative marker Calnexin. (d) Representative images of HUVECs tube formation after treatment with DMEM, BC-derived EVs, or MSC-derived EVs. Scale bar, 100 μm. (e) Quantification of the number of tubes formed in each group (n = 5 technical replicates). (f) Cell viability of BCs cultured under serum-depleted conditions and treated with DMEM, or increasing concentrations of BC-EVs or MSC-EVs (n = 3 technical replicates). (e) and (f) All data are presented as mean ± SEM. Statistical analysis was performed using a one-way ANOVA with Tukey's multiple comparisons test. ∗∗ P < 0.01, ∗∗∗ P < 0.001, ∗∗∗∗ P < 0.0001; ns, not significant.

Article Snippet: Human umbilical vein endothelial cells (HUVECs) were obtained from the American Type Culture Collection (ATCC) and cultured in DMEM supplemented with 10 % fetal bovine serum.

Techniques: Transmission Assay, Electron Microscopy, Flow Cytometry, Western Blot, Expressing, Marker, Derivative Assay, Cell Culture

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: (A) Effects of different concentrations of rosuvastatin (0.1, 1, 5 and 10 µM) on HUVEC viability for 24 h. (B) Effects of treatment with different concentrations of ox-LDL (50, 100 and 200 µg/mL) for 24 h on HUVEC viability. (C) HUVECs were treated with different concentrations of rosuvastatin and ox-LDL (200 µg/ml) for 24 h. * P < 0.05, *** P < 0.001 by one-way ANOVA. (D) Bar chart showing the signaling pathways enriched with DEGs in the RNA-Seq dataset ( GSE206927 ) of ox-LDL-treated HUVECs according to GO analysis. (E) Bubble chart showing the signaling pathways enriched with DEGs according to KEGG analysis. (F-G) HUVECs stimulated with ox-LDL and different concentrations of rosuvastatin were stained with DAPI (blue) and Ki67 (purple). Ki67-positive cells were quantified, bar = 100 μm, * P < 0.05, **** P < 0.0001 by one-way ANOVA.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Protein-Protein interactions, RNA Sequencing, Staining

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: HUVECs were treated with ox-LDL in the presence or absence of different concentrations of rosuvastatin (0.1, 1, 5 and 10 µM) for 24 h. (A) NO production in HUVECs. (B) eNOS mRNA expression in HUVECs. (C) A microplate reader was used to measure the fluorescence intensity of the ROS at an excitation wavelength of 488 nm and an absorption wavelength of 525 nm via a fluorescent probe DCFH-DA kit, and Rosup was used as a positive control. (D) The mean intracellular fluorescence intensity was analyzed via fluorescence microscopy. The data are presented as the mean ± SEM. * P < 0.05, ** P < 0.01, ** P < 0.0001 by one-way ANOVA.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Expressing, Fluorescence, Positive Control, Microscopy

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: (A-B) Bcl2 and Bax mRNA expression in HUVECs treated with different concentrations of rosuvastatin and ox-LDL (200 µg/ml) for 24 h. ** P < 0.01, *** P < 0.001, **** P < 0.0001 by one-way ANOVA. (C-D) BCL-2 and Bax protein expression in HUVECs treated with different concentrations of rosuvastatin and ox-LDL (200 µg/ml) for 24 h. The data are presented as the means ± SEMs. * P < 0.05 by one-way ANOVA. (E) HUVECs stimulated with ox-LDL and different concentrations of rosuvastatin were stained with DAPI (blue), Bax (green) and mitochondria (red); scale bar = 20 μm. (F) Early and late apoptosis of HUVECs treated with 100 µg/mL ox-LDL and 10 μmol/L rosuvastatin for 24 h. The quantification results are shown on the right (n = 5). *** P < 0.001, **** P < 0.0001 by one-way ANOVA.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Expressing, Staining

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: (A-D) Protein levels of IkBα, p-IkBα, P65 and p-P65 in HUVECs treated with or without 10 µM rosuvastatin and treated with 100 µg/mL ox-LDL for 24 h. The data are presented as the means ± SEMs. * P < 0.05, ** P < 0.01 by one-way ANOVA. (E) Schematic diagram illustrating the role of rosuvastatin in ox-LDL-induced endothelial cell dysfunction. Rosuvastatin regulates oxidative stress and apoptosis-related gene transcription in endothelial cells by inhibiting ox-LDL-induced IKBα and P65 activation in endothelial cells.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Activation Assay