human dermal lymphatic endothelial cells (hdlecs) Search Results


96
PromoCell human dermal lymphatic endothelial cells
(A) Conceptual abstract: The vessel-chip provides a versatile platform to model <t>endothelial</t> dysfunction in the context of SARS-CoV-2 infection by incorporating physiological flow, vascular cells, and circulating blood factors. Using this system, we probed the distinct and interactive impacts of flow, inflammatory cytokine IL-6, and viral proteins on endothelial integrity. ( B) Schematic of the microchannel design (vessel-chip) with an inlet, a straight duct 200 μm wide and 75 μm high, and an outlet. ( C) Photograph of a representative vessel-chip used in experiments. ( D) A micrograph of endothelial lining (HAECs) inside the vessel chip stained for Actin (red), VE-cadherin (green), and nuclei (DAPI, blue); scale bar: 200 μm. ( E) Confocal micrograph showing a sectional view of endothelial lumen formed by HAECs in the microchannel. Orthogonal projections (top ‘xy’; front ‘xz’, side ‘yz’) confirm complete HAEC coverage across all four channel walls (red: Actin; green: VE-cadherin; blue: nuclei); scale bar: 50 μm.
Human Dermal Lymphatic Endothelial Cells, supplied by PromoCell, 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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94
PromoCell human dermal lymphatic ecs
In the microvasculature, the arterial endothelium is iron depleted. (A) UMAP and principal component analysis plots of previously published single-cell RNA sequencing (scRNA-seq) of human <t>ECs</t> reanalyzed with pseudobulk analysis. Statistical analysis was performed with DESeq2. (B) Expression of FTH1 and FTL in previously published scRNA-seq data of human ECs from males (blue) and females (pink). (C-D) Ferritin heavy chain ( Fth1 ) and transferrin receptor ( Tfrc ) expression in previously published scRNA-seq data of ECs isolated from adipose and mesentery. ∗ P < .0001 vs artery; # P < .0001 vs capillary; & P < .0001 vs vein. Statistical analysis was performed with Wilcoxon rank-sum test. (E) Mesenteric endothelial labile iron assessed with FerroOrange by flow cytometry. Statistical analysis was performed with paired t test. (F-J) Human coronary artery ECs and human <t>dermal</t> <t>lymphatic</t> ECs were treated with DFO or vehicle control for 24 hours; labile iron was assessed with FerroOrange by flow cytometry (F) and microscopy (G; scale bar, 50 μm); and FTH was assessed by western blot (H). Statistical analysis was performed with 2-way analysis of variance (ANOVA) and Holms-Šídák post hoc analysis. (I-J) The expression of SOX17 , PROX1 , and markers of arterial and lymphatic EC phenotypes were assessed by bulk RNA sequencing. Statistical analysis was performed with DESeq2. ∗ P < .05. AEC, arterial ECs; Avg Exp, average expression; BEC, blood ECs; Con, control; LEC, lymphatic ECs; MFI, mean fluorescence intensity; PC, principal component; Pct Exp, percent expressed; UMAP, uniform manifold and projection.
Human Dermal Lymphatic Ecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+dermal+lymphatic+endothelial+cells+(hdlecs)/Human+Dermal+Lymphatic+Endothelial+Cells+(HDLEC)+adult+donor/pmc13675883-28-12-17
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human dermal lymphatic ecs - by Bioz Stars, 2026-10
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90
ScienCell human dermal lymphatic endothelial cells (hdlecs)
(A): HMGB1 promoted VEGF-C-induced <t>HDLECs</t> proliferation in a dose-dependent manner. (B): TLR4 mediates HMGB1-induced LECs proliferation. (C-E): TLR4 mediates HMGB1-induced LECs tube formation.* p < 0.05, ** p < 0.01, *** p < 0.001
Human Dermal Lymphatic Endothelial Cells (Hdlecs), supplied by ScienCell, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+dermal+lymphatic+endothelial+cells+(hdlecs)/human+dermal+lymphatic+endothelial+cells++hdlecs+/pmc04839690-61-0-9
Average 90 stars, based on 1 article reviews
human dermal lymphatic endothelial cells (hdlecs) - by Bioz Stars, 2026-10
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90
Avantor human dermal lymphatic endothelial cells (hdlecs
(A): HMGB1 promoted VEGF-C-induced <t>HDLECs</t> proliferation in a dose-dependent manner. (B): TLR4 mediates HMGB1-induced LECs proliferation. (C-E): TLR4 mediates HMGB1-induced LECs tube formation.* p < 0.05, ** p < 0.01, *** p < 0.001
Human Dermal Lymphatic Endothelial Cells (Hdlecs, supplied by Avantor, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/human+dermal+lymphatic+endothelial+cells+(hdlecs)/human+dermal+lymphatic+endothelial+cells++hdlecs/pmc10706153-81-0-6
Average 90 stars, based on 1 article reviews
human dermal lymphatic endothelial cells (hdlecs - by Bioz Stars, 2026-10
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(A) Conceptual abstract: The vessel-chip provides a versatile platform to model endothelial dysfunction in the context of SARS-CoV-2 infection by incorporating physiological flow, vascular cells, and circulating blood factors. Using this system, we probed the distinct and interactive impacts of flow, inflammatory cytokine IL-6, and viral proteins on endothelial integrity. ( B) Schematic of the microchannel design (vessel-chip) with an inlet, a straight duct 200 μm wide and 75 μm high, and an outlet. ( C) Photograph of a representative vessel-chip used in experiments. ( D) A micrograph of endothelial lining (HAECs) inside the vessel chip stained for Actin (red), VE-cadherin (green), and nuclei (DAPI, blue); scale bar: 200 μm. ( E) Confocal micrograph showing a sectional view of endothelial lumen formed by HAECs in the microchannel. Orthogonal projections (top ‘xy’; front ‘xz’, side ‘yz’) confirm complete HAEC coverage across all four channel walls (red: Actin; green: VE-cadherin; blue: nuclei); scale bar: 50 μm.

Journal: Journal of thrombosis and haemostasis : JTH

Article Title: Shear–cytokine crosstalk is a determinant of SARS-CoV-2 induced endothelial pathophysiology and thrombosis in human vessel-chips

doi: 10.1016/j.jtha.2026.04.034

Figure Lengend Snippet: (A) Conceptual abstract: The vessel-chip provides a versatile platform to model endothelial dysfunction in the context of SARS-CoV-2 infection by incorporating physiological flow, vascular cells, and circulating blood factors. Using this system, we probed the distinct and interactive impacts of flow, inflammatory cytokine IL-6, and viral proteins on endothelial integrity. ( B) Schematic of the microchannel design (vessel-chip) with an inlet, a straight duct 200 μm wide and 75 μm high, and an outlet. ( C) Photograph of a representative vessel-chip used in experiments. ( D) A micrograph of endothelial lining (HAECs) inside the vessel chip stained for Actin (red), VE-cadherin (green), and nuclei (DAPI, blue); scale bar: 200 μm. ( E) Confocal micrograph showing a sectional view of endothelial lumen formed by HAECs in the microchannel. Orthogonal projections (top ‘xy’; front ‘xz’, side ‘yz’) confirm complete HAEC coverage across all four channel walls (red: Actin; green: VE-cadherin; blue: nuclei); scale bar: 50 μm.

Article Snippet: Human aortic endothelial cells (HAECs; Lonza , CC-2535) and human dermal lymphatic endothelial cells (HDLECs; Promocell , C-12216) were cultured in Endothelial Cell Growth Medium MV2 (EGM-2MV; Lonza , CC-3202).

Techniques: Infection, Staining, Confocal

(A) (i) Endothelialized vessel-chips lined with three different cell types, HUVECs, HAECs, and HDLECs, were exposed to VSV-ΔG-Spike for 24 hours. (ii) post-treatment analyses included gap area, cell orientation, cell circularity, and VE-cadherin fluorescence intensity as a measure of barrier integrity. (B–D) Characterization of HUVECs, HAECs, and HDLECs, respectively, after spike protein treatment: (i) representative micrographs (white arrows indicate gaps within the monolayer); (ii) quantification of gap area; (iii) VE-cadherin fluorescence intensity (barrier integrity); (iv) cell circularity; (v) cell orientation; and (vi) orientation distribution plotted as polar plots. (E) Relative differences between treated and untreated groups, calculated as (treated – untreated), for each cell type: (i) gap area, (ii) VE-cadherin fluorescence intensity (barrier integrity), (iii) cell circularity, and (iv) cell orientation distribution in polar plots; Concentrations: VSV-ΔG-Spike :10 MOI; scale bar: 50 μm. Statistics: NS: not significant, *p < 0.05, n = 3 devices for all experiments.

Journal: Journal of thrombosis and haemostasis : JTH

Article Title: Shear–cytokine crosstalk is a determinant of SARS-CoV-2 induced endothelial pathophysiology and thrombosis in human vessel-chips

doi: 10.1016/j.jtha.2026.04.034

Figure Lengend Snippet: (A) (i) Endothelialized vessel-chips lined with three different cell types, HUVECs, HAECs, and HDLECs, were exposed to VSV-ΔG-Spike for 24 hours. (ii) post-treatment analyses included gap area, cell orientation, cell circularity, and VE-cadherin fluorescence intensity as a measure of barrier integrity. (B–D) Characterization of HUVECs, HAECs, and HDLECs, respectively, after spike protein treatment: (i) representative micrographs (white arrows indicate gaps within the monolayer); (ii) quantification of gap area; (iii) VE-cadherin fluorescence intensity (barrier integrity); (iv) cell circularity; (v) cell orientation; and (vi) orientation distribution plotted as polar plots. (E) Relative differences between treated and untreated groups, calculated as (treated – untreated), for each cell type: (i) gap area, (ii) VE-cadherin fluorescence intensity (barrier integrity), (iii) cell circularity, and (iv) cell orientation distribution in polar plots; Concentrations: VSV-ΔG-Spike :10 MOI; scale bar: 50 μm. Statistics: NS: not significant, *p < 0.05, n = 3 devices for all experiments.

Article Snippet: Human aortic endothelial cells (HAECs; Lonza , CC-2535) and human dermal lymphatic endothelial cells (HDLECs; Promocell , C-12216) were cultured in Endothelial Cell Growth Medium MV2 (EGM-2MV; Lonza , CC-3202).

Techniques: Fluorescence

(A) Schematic representation and representative micrographs of experimental conditions: (i) control endothelialized vessel without treatment, (ii) VSV-ΔG-Spike alone in the absence of flow and/or IL-6, (iii) VSV-ΔG-Spike with flow, (iv) VSV-ΔG-Spike with IL-6, and (v) VSV-ΔG-Spike with IL-6 under flow. (B) Micrographs of endothelialized vessels infected with VSV-ΔG-Spike carrying an enhanced green fluorescent protein (eGFP) reporter, visualized to assess viral replication in each condition. (C) Micrographs of whole blood, with platelets (red) and fibrin (green), perfused through endothelialized channels subjected to each treatment condition. (D) Quantitative analyses: (i) GFP fluorescence indicating VSV-ΔG-Spike replication across conditions, (ii) fibrin coverage, and (iii) platelet coverage after blood perfusion under the specified treatment groups; Concentrations: VSV-ΔG-Spike :10 MOI; scale bar: 200 μm. Statistics: NS: not significant, *p < 0.05, n = 3 devices for all experiments.

Journal: Journal of thrombosis and haemostasis : JTH

Article Title: Shear–cytokine crosstalk is a determinant of SARS-CoV-2 induced endothelial pathophysiology and thrombosis in human vessel-chips

doi: 10.1016/j.jtha.2026.04.034

Figure Lengend Snippet: (A) Schematic representation and representative micrographs of experimental conditions: (i) control endothelialized vessel without treatment, (ii) VSV-ΔG-Spike alone in the absence of flow and/or IL-6, (iii) VSV-ΔG-Spike with flow, (iv) VSV-ΔG-Spike with IL-6, and (v) VSV-ΔG-Spike with IL-6 under flow. (B) Micrographs of endothelialized vessels infected with VSV-ΔG-Spike carrying an enhanced green fluorescent protein (eGFP) reporter, visualized to assess viral replication in each condition. (C) Micrographs of whole blood, with platelets (red) and fibrin (green), perfused through endothelialized channels subjected to each treatment condition. (D) Quantitative analyses: (i) GFP fluorescence indicating VSV-ΔG-Spike replication across conditions, (ii) fibrin coverage, and (iii) platelet coverage after blood perfusion under the specified treatment groups; Concentrations: VSV-ΔG-Spike :10 MOI; scale bar: 200 μm. Statistics: NS: not significant, *p < 0.05, n = 3 devices for all experiments.

Article Snippet: Human aortic endothelial cells (HAECs; Lonza , CC-2535) and human dermal lymphatic endothelial cells (HDLECs; Promocell , C-12216) were cultured in Endothelial Cell Growth Medium MV2 (EGM-2MV; Lonza , CC-3202).

Techniques: Control, Infection, Fluorescence

(A) Schematic representation and micrographs of experimental conditions: (i) VSV-ΔG-Spike treated (ii) SARS-CoV-2 treated; white arrows indicate gaps within the monolayer (B) Quantitative analysis of (i) gap area, (ii) VE-cadherin fluorescence intensity (barrier integrity), (iii) cell circularity, (iv) cell orientation, and (v) cell orientation distribution in polar plots; scale bar: 50 μm (C) (i) Endothelial activation quantified by measuring ICAM-1 fluorescence intensity and expressing values as percent change relative to untreated control. (ii) Micrographs of endothelialized vessels immunostained for ICAM-1 under untreated condition and following VSV-ΔG-Spike or SARS-CoV-2 exposure; scale bar: 200 μm (D) Quantitative analyses: (i) GFP fluorescence indicating VSV-ΔG-Spike and SARS-CoV-2 replication across conditions (ii) Micrographs of endothelialized vessels infected with VSV-ΔG-Spike and SARS-CoV-2 carrying an enhanced green fluorescent protein (GFP) reporter, visualized to assess viral replication in each condition; Concentrations: VSV-ΔG-Spike and SARS-CoV-2 :10 MOI; scale bar: 200 μm. Statistics: NS: not significant, *p < 0.05, n = 3 devices for all experiments.

Journal: Journal of thrombosis and haemostasis : JTH

Article Title: Shear–cytokine crosstalk is a determinant of SARS-CoV-2 induced endothelial pathophysiology and thrombosis in human vessel-chips

doi: 10.1016/j.jtha.2026.04.034

Figure Lengend Snippet: (A) Schematic representation and micrographs of experimental conditions: (i) VSV-ΔG-Spike treated (ii) SARS-CoV-2 treated; white arrows indicate gaps within the monolayer (B) Quantitative analysis of (i) gap area, (ii) VE-cadherin fluorescence intensity (barrier integrity), (iii) cell circularity, (iv) cell orientation, and (v) cell orientation distribution in polar plots; scale bar: 50 μm (C) (i) Endothelial activation quantified by measuring ICAM-1 fluorescence intensity and expressing values as percent change relative to untreated control. (ii) Micrographs of endothelialized vessels immunostained for ICAM-1 under untreated condition and following VSV-ΔG-Spike or SARS-CoV-2 exposure; scale bar: 200 μm (D) Quantitative analyses: (i) GFP fluorescence indicating VSV-ΔG-Spike and SARS-CoV-2 replication across conditions (ii) Micrographs of endothelialized vessels infected with VSV-ΔG-Spike and SARS-CoV-2 carrying an enhanced green fluorescent protein (GFP) reporter, visualized to assess viral replication in each condition; Concentrations: VSV-ΔG-Spike and SARS-CoV-2 :10 MOI; scale bar: 200 μm. Statistics: NS: not significant, *p < 0.05, n = 3 devices for all experiments.

Article Snippet: Human aortic endothelial cells (HAECs; Lonza , CC-2535) and human dermal lymphatic endothelial cells (HDLECs; Promocell , C-12216) were cultured in Endothelial Cell Growth Medium MV2 (EGM-2MV; Lonza , CC-3202).

Techniques: Comparison, Analysis, Fluorescence, Activation Assay, Expressing, Control, Infection

In the microvasculature, the arterial endothelium is iron depleted. (A) UMAP and principal component analysis plots of previously published single-cell RNA sequencing (scRNA-seq) of human ECs reanalyzed with pseudobulk analysis. Statistical analysis was performed with DESeq2. (B) Expression of FTH1 and FTL in previously published scRNA-seq data of human ECs from males (blue) and females (pink). (C-D) Ferritin heavy chain ( Fth1 ) and transferrin receptor ( Tfrc ) expression in previously published scRNA-seq data of ECs isolated from adipose and mesentery. ∗ P < .0001 vs artery; # P < .0001 vs capillary; & P < .0001 vs vein. Statistical analysis was performed with Wilcoxon rank-sum test. (E) Mesenteric endothelial labile iron assessed with FerroOrange by flow cytometry. Statistical analysis was performed with paired t test. (F-J) Human coronary artery ECs and human dermal lymphatic ECs were treated with DFO or vehicle control for 24 hours; labile iron was assessed with FerroOrange by flow cytometry (F) and microscopy (G; scale bar, 50 μm); and FTH was assessed by western blot (H). Statistical analysis was performed with 2-way analysis of variance (ANOVA) and Holms-Šídák post hoc analysis. (I-J) The expression of SOX17 , PROX1 , and markers of arterial and lymphatic EC phenotypes were assessed by bulk RNA sequencing. Statistical analysis was performed with DESeq2. ∗ P < .05. AEC, arterial ECs; Avg Exp, average expression; BEC, blood ECs; Con, control; LEC, lymphatic ECs; MFI, mean fluorescence intensity; PC, principal component; Pct Exp, percent expressed; UMAP, uniform manifold and projection.

Journal: Blood

Article Title: Arterial iron regulates vasodilation during anemia via endothelial holo-α-globin

doi: 10.1182/blood.2025032905

Figure Lengend Snippet: In the microvasculature, the arterial endothelium is iron depleted. (A) UMAP and principal component analysis plots of previously published single-cell RNA sequencing (scRNA-seq) of human ECs reanalyzed with pseudobulk analysis. Statistical analysis was performed with DESeq2. (B) Expression of FTH1 and FTL in previously published scRNA-seq data of human ECs from males (blue) and females (pink). (C-D) Ferritin heavy chain ( Fth1 ) and transferrin receptor ( Tfrc ) expression in previously published scRNA-seq data of ECs isolated from adipose and mesentery. ∗ P < .0001 vs artery; # P < .0001 vs capillary; & P < .0001 vs vein. Statistical analysis was performed with Wilcoxon rank-sum test. (E) Mesenteric endothelial labile iron assessed with FerroOrange by flow cytometry. Statistical analysis was performed with paired t test. (F-J) Human coronary artery ECs and human dermal lymphatic ECs were treated with DFO or vehicle control for 24 hours; labile iron was assessed with FerroOrange by flow cytometry (F) and microscopy (G; scale bar, 50 μm); and FTH was assessed by western blot (H). Statistical analysis was performed with 2-way analysis of variance (ANOVA) and Holms-Šídák post hoc analysis. (I-J) The expression of SOX17 , PROX1 , and markers of arterial and lymphatic EC phenotypes were assessed by bulk RNA sequencing. Statistical analysis was performed with DESeq2. ∗ P < .05. AEC, arterial ECs; Avg Exp, average expression; BEC, blood ECs; Con, control; LEC, lymphatic ECs; MFI, mean fluorescence intensity; PC, principal component; Pct Exp, percent expressed; UMAP, uniform manifold and projection.

Article Snippet: To deplete iron, human coronary artery ECs (CC-2585; Lonza, Basel, Switzerland) and human dermal lymphatic ECs (C-12217; PromoCell, Heidelberg, Germany) were plated at a seeding density of 167 × 10 3 cells per well in a 6-well plate.

Techniques: Analysis, Single Cell, RNA Sequencing, Expressing, Isolation, Flow Cytometry, Control, Microscopy, Western Blot, Bulk RNA Sequencing, Fluorescence

(A): HMGB1 promoted VEGF-C-induced HDLECs proliferation in a dose-dependent manner. (B): TLR4 mediates HMGB1-induced LECs proliferation. (C-E): TLR4 mediates HMGB1-induced LECs tube formation.* p < 0.05, ** p < 0.01, *** p < 0.001

Journal: PLoS ONE

Article Title: High Mobility Group Box-1 Promotes Inflammation-Induced Lymphangiogenesis via Toll-Like Receptor 4-Dependent Signalling Pathway

doi: 10.1371/journal.pone.0154187

Figure Lengend Snippet: (A): HMGB1 promoted VEGF-C-induced HDLECs proliferation in a dose-dependent manner. (B): TLR4 mediates HMGB1-induced LECs proliferation. (C-E): TLR4 mediates HMGB1-induced LECs tube formation.* p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Human dermal lymphatic endothelial cells (HDLECs) were purchased from ScienCell (Carlsbad, CA) and maintained in endothelial cell basal medium-2 with growth supplements (EBM-2 MV).

Techniques: