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human dermal microvascular endothelial cells (hdmecs; cat #2000  (ScienCell)

 
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    ScienCell human dermal microvascular endothelial cells (hdmecs; cat #2000
    Expression of CD123 in HUVECs. ( A ) Surface expression of CD123 MFI on HUVECs and HDVECs was detected by staining with anti-CD123 APC and flow cytometry in Accuri C6. Representative plots are shown. ( B ) Expression of CD123 on HUVECs after treatment with cytokines (IL-1α, IL-1β, IL-4, IL-6, TNF-α, and IFN-γ) for 24 hrs was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. ( C-D ) Expression of CD123 on HUVECs after treatment with IFN-γ, TNF-α ( C ), and IL-4 ( D ) at different concentrations for different time points (mean±SEM, n=3). Data show one representative experiment. ( E ) In HUVECs, the expression of CD123 after treated with IFN-γ, TNF-α, and IL-4 for 24 hrs was detected by mRNA Microarray Analysis (mean ± SEM of triplicate). ( F ) Expression of CD123 on HDMECs after treatment with IFN-γ, TNF-α, and IL-4 for 24h was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. * P <0.05; *** P <0.001; **** P <0.0001. Abbreviations: MFI, mean fluorescence intensity; IFN, interferon; TNF, tumor necrosis factor, HUVECs, human umbilical vein endothelial cells; HDMECs, human dermal <t>microvascular</t> endothelial cells.
    Human Dermal Microvascular Endothelial Cells (Hdmecs; Cat #2000, 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/hdmecs+2000/pmc06600319-35-40-48?v=ScienCell
    Average 90 stars, based on 1 article reviews
    human dermal microvascular endothelial cells (hdmecs; cat #2000 - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "IFN-γ and TNF-α aggravate endothelial damage caused by CD123-targeted CAR T cell"

    Article Title: IFN-γ and TNF-α aggravate endothelial damage caused by CD123-targeted CAR T cell

    Journal: OncoTargets and therapy

    doi: 10.2147/OTT.S205678

    Expression of CD123 in HUVECs. ( A ) Surface expression of CD123 MFI on HUVECs and HDVECs was detected by staining with anti-CD123 APC and flow cytometry in Accuri C6. Representative plots are shown. ( B ) Expression of CD123 on HUVECs after treatment with cytokines (IL-1α, IL-1β, IL-4, IL-6, TNF-α, and IFN-γ) for 24 hrs was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. ( C-D ) Expression of CD123 on HUVECs after treatment with IFN-γ, TNF-α ( C ), and IL-4 ( D ) at different concentrations for different time points (mean±SEM, n=3). Data show one representative experiment. ( E ) In HUVECs, the expression of CD123 after treated with IFN-γ, TNF-α, and IL-4 for 24 hrs was detected by mRNA Microarray Analysis (mean ± SEM of triplicate). ( F ) Expression of CD123 on HDMECs after treatment with IFN-γ, TNF-α, and IL-4 for 24h was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. * P <0.05; *** P <0.001; **** P <0.0001. Abbreviations: MFI, mean fluorescence intensity; IFN, interferon; TNF, tumor necrosis factor, HUVECs, human umbilical vein endothelial cells; HDMECs, human dermal microvascular endothelial cells.
    Figure Legend Snippet: Expression of CD123 in HUVECs. ( A ) Surface expression of CD123 MFI on HUVECs and HDVECs was detected by staining with anti-CD123 APC and flow cytometry in Accuri C6. Representative plots are shown. ( B ) Expression of CD123 on HUVECs after treatment with cytokines (IL-1α, IL-1β, IL-4, IL-6, TNF-α, and IFN-γ) for 24 hrs was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. ( C-D ) Expression of CD123 on HUVECs after treatment with IFN-γ, TNF-α ( C ), and IL-4 ( D ) at different concentrations for different time points (mean±SEM, n=3). Data show one representative experiment. ( E ) In HUVECs, the expression of CD123 after treated with IFN-γ, TNF-α, and IL-4 for 24 hrs was detected by mRNA Microarray Analysis (mean ± SEM of triplicate). ( F ) Expression of CD123 on HDMECs after treatment with IFN-γ, TNF-α, and IL-4 for 24h was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. * P <0.05; *** P <0.001; **** P <0.0001. Abbreviations: MFI, mean fluorescence intensity; IFN, interferon; TNF, tumor necrosis factor, HUVECs, human umbilical vein endothelial cells; HDMECs, human dermal microvascular endothelial cells.

    Techniques Used: Expressing, Staining, Flow Cytometry, Microarray, Fluorescence



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    human dermal microvascular endothelial cells (hdmecs; cat #2000  (ScienCell)
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    ScienCell human dermal microvascular endothelial cells (hdmecs; cat #2000
    Expression of CD123 in HUVECs. ( A ) Surface expression of CD123 MFI on HUVECs and HDVECs was detected by staining with anti-CD123 APC and flow cytometry in Accuri C6. Representative plots are shown. ( B ) Expression of CD123 on HUVECs after treatment with cytokines (IL-1α, IL-1β, IL-4, IL-6, TNF-α, and IFN-γ) for 24 hrs was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. ( C-D ) Expression of CD123 on HUVECs after treatment with IFN-γ, TNF-α ( C ), and IL-4 ( D ) at different concentrations for different time points (mean±SEM, n=3). Data show one representative experiment. ( E ) In HUVECs, the expression of CD123 after treated with IFN-γ, TNF-α, and IL-4 for 24 hrs was detected by mRNA Microarray Analysis (mean ± SEM of triplicate). ( F ) Expression of CD123 on HDMECs after treatment with IFN-γ, TNF-α, and IL-4 for 24h was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. * P <0.05; *** P <0.001; **** P <0.0001. Abbreviations: MFI, mean fluorescence intensity; IFN, interferon; TNF, tumor necrosis factor, HUVECs, human umbilical vein endothelial cells; HDMECs, human dermal <t>microvascular</t> endothelial cells.
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    High levels of barrier resistance correlate with continuous intercellular junctions and cortical arrangement of the actin cytoskeleton. (A) Confocal images of confluent endothelial monolayers displayed in order of low (HAEC, HBMVEC, and HUVEC) and high levels of barrier resistance (HLMVEC and HDMEC) left to right (bar, 20 µm; representative of n = 3). HLMVEC and HDMEC exhibit a linear and organized junctional staining of VE-cadherin, claudin-5, and ZO-1 compared with an irregular junctional pattern in cell types with lower levels of resistance. Phalloidin staining reveals a strict cortical arrangement of the actin cytoskeleton in HLMVEC and HDMEC, whereas cells with low resistance exhibit more stress fibers. Localization of cortactin is more peripheral and less cytoplasmic <t>in</t> <t>HLMVECs</t> and <t>HDMECs.</t> F-actin fibers aligned along the cell periphery, minimizing radial tension forces at cell junctions, indicated by linear junctional pattern of VE-cadherin/phalloidin overlay images (arrows) and lower presence of pMLC2 in HLMVECs and HDMECs. ( B–F) Graphs presenting mean values of fluorescence intensity across multiple cell–cell junctions per cell type (Fig. S2 B) for each barrier protein shown in A. Junctional components as well as phalloidin and cortactin are concentrated along the cell borders in HLMVECs and HDMECs compared with cell types with low barrier resistance.
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    human dermal microvascular endothelial cells (hdmecs; cat. no. 2000)  (ScienCell)
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    ScienCell human dermal microvascular endothelial cells (hdmecs; cat. no. 2000)
    High levels of barrier resistance correlate with continuous intercellular junctions and cortical arrangement of the actin cytoskeleton. (A) Confocal images of confluent endothelial monolayers displayed in order of low (HAEC, HBMVEC, and HUVEC) and high levels of barrier resistance (HLMVEC and HDMEC) left to right (bar, 20 µm; representative of n = 3). HLMVEC and HDMEC exhibit a linear and organized junctional staining of VE-cadherin, claudin-5, and ZO-1 compared with an irregular junctional pattern in cell types with lower levels of resistance. Phalloidin staining reveals a strict cortical arrangement of the actin cytoskeleton in HLMVEC and HDMEC, whereas cells with low resistance exhibit more stress fibers. Localization of cortactin is more peripheral and less cytoplasmic <t>in</t> <t>HLMVECs</t> and <t>HDMECs.</t> F-actin fibers aligned along the cell periphery, minimizing radial tension forces at cell junctions, indicated by linear junctional pattern of VE-cadherin/phalloidin overlay images (arrows) and lower presence of pMLC2 in HLMVECs and HDMECs. ( B–F) Graphs presenting mean values of fluorescence intensity across multiple cell–cell junctions per cell type (Fig. S2 B) for each barrier protein shown in A. Junctional components as well as phalloidin and cortactin are concentrated along the cell borders in HLMVECs and HDMECs compared with cell types with low barrier resistance.
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    High levels of barrier resistance correlate with continuous intercellular junctions and cortical arrangement of the actin cytoskeleton. (A) Confocal images of confluent endothelial monolayers displayed in order of low (HAEC, HBMVEC, and HUVEC) and high levels of barrier resistance (HLMVEC and HDMEC) left to right (bar, 20 µm; representative of n = 3). HLMVEC and HDMEC exhibit a linear and organized junctional staining of VE-cadherin, claudin-5, and ZO-1 compared with an irregular junctional pattern in cell types with lower levels of resistance. Phalloidin staining reveals a strict cortical arrangement of the actin cytoskeleton in HLMVEC and HDMEC, whereas cells with low resistance exhibit more stress fibers. Localization of cortactin is more peripheral and less cytoplasmic <t>in</t> <t>HLMVECs</t> and <t>HDMECs.</t> F-actin fibers aligned along the cell periphery, minimizing radial tension forces at cell junctions, indicated by linear junctional pattern of VE-cadherin/phalloidin overlay images (arrows) and lower presence of pMLC2 in HLMVECs and HDMECs. ( B–F) Graphs presenting mean values of fluorescence intensity across multiple cell–cell junctions per cell type (Fig. S2 B) for each barrier protein shown in A. Junctional components as well as phalloidin and cortactin are concentrated along the cell borders in HLMVECs and HDMECs compared with cell types with low barrier resistance.
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    Image Search Results


    Expression of CD123 in HUVECs. ( A ) Surface expression of CD123 MFI on HUVECs and HDVECs was detected by staining with anti-CD123 APC and flow cytometry in Accuri C6. Representative plots are shown. ( B ) Expression of CD123 on HUVECs after treatment with cytokines (IL-1α, IL-1β, IL-4, IL-6, TNF-α, and IFN-γ) for 24 hrs was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. ( C-D ) Expression of CD123 on HUVECs after treatment with IFN-γ, TNF-α ( C ), and IL-4 ( D ) at different concentrations for different time points (mean±SEM, n=3). Data show one representative experiment. ( E ) In HUVECs, the expression of CD123 after treated with IFN-γ, TNF-α, and IL-4 for 24 hrs was detected by mRNA Microarray Analysis (mean ± SEM of triplicate). ( F ) Expression of CD123 on HDMECs after treatment with IFN-γ, TNF-α, and IL-4 for 24h was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. * P <0.05; *** P <0.001; **** P <0.0001. Abbreviations: MFI, mean fluorescence intensity; IFN, interferon; TNF, tumor necrosis factor, HUVECs, human umbilical vein endothelial cells; HDMECs, human dermal microvascular endothelial cells.

    Journal: OncoTargets and therapy

    Article Title: IFN-γ and TNF-α aggravate endothelial damage caused by CD123-targeted CAR T cell

    doi: 10.2147/OTT.S205678

    Figure Lengend Snippet: Expression of CD123 in HUVECs. ( A ) Surface expression of CD123 MFI on HUVECs and HDVECs was detected by staining with anti-CD123 APC and flow cytometry in Accuri C6. Representative plots are shown. ( B ) Expression of CD123 on HUVECs after treatment with cytokines (IL-1α, IL-1β, IL-4, IL-6, TNF-α, and IFN-γ) for 24 hrs was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. ( C-D ) Expression of CD123 on HUVECs after treatment with IFN-γ, TNF-α ( C ), and IL-4 ( D ) at different concentrations for different time points (mean±SEM, n=3). Data show one representative experiment. ( E ) In HUVECs, the expression of CD123 after treated with IFN-γ, TNF-α, and IL-4 for 24 hrs was detected by mRNA Microarray Analysis (mean ± SEM of triplicate). ( F ) Expression of CD123 on HDMECs after treatment with IFN-γ, TNF-α, and IL-4 for 24h was detected by flow cytometry (mean±SEM, n=3). Data show one representative experiment. * P <0.05; *** P <0.001; **** P <0.0001. Abbreviations: MFI, mean fluorescence intensity; IFN, interferon; TNF, tumor necrosis factor, HUVECs, human umbilical vein endothelial cells; HDMECs, human dermal microvascular endothelial cells.

    Article Snippet: AML cell lines KG-1a and MOLM-13 (ATCC, USA), chronic myelogenous leukemia (CML) cell line K562 (ATCC, USA), B-cell acute lymphoblastic leukemia (B-ALL) cell line NALM-6 (ATCC, USA), human umbilical vein endothelial cells (HUVECs; Cat #8000, ScienCell, USA) before passage 7, human dermal microvascular endothelial cells (HDMECs; Cat #2000, ScienCell, USA) before passage 5, primary AML cells (AML-2 and AML-3), and healthy donor-derived blood samples were used in the current study.

    Techniques: Expressing, Staining, Flow Cytometry, Microarray, Fluorescence

    High levels of barrier resistance correlate with continuous intercellular junctions and cortical arrangement of the actin cytoskeleton. (A) Confocal images of confluent endothelial monolayers displayed in order of low (HAEC, HBMVEC, and HUVEC) and high levels of barrier resistance (HLMVEC and HDMEC) left to right (bar, 20 µm; representative of n = 3). HLMVEC and HDMEC exhibit a linear and organized junctional staining of VE-cadherin, claudin-5, and ZO-1 compared with an irregular junctional pattern in cell types with lower levels of resistance. Phalloidin staining reveals a strict cortical arrangement of the actin cytoskeleton in HLMVEC and HDMEC, whereas cells with low resistance exhibit more stress fibers. Localization of cortactin is more peripheral and less cytoplasmic in HLMVECs and HDMECs. F-actin fibers aligned along the cell periphery, minimizing radial tension forces at cell junctions, indicated by linear junctional pattern of VE-cadherin/phalloidin overlay images (arrows) and lower presence of pMLC2 in HLMVECs and HDMECs. ( B–F) Graphs presenting mean values of fluorescence intensity across multiple cell–cell junctions per cell type (Fig. S2 B) for each barrier protein shown in A. Junctional components as well as phalloidin and cortactin are concentrated along the cell borders in HLMVECs and HDMECs compared with cell types with low barrier resistance.

    Journal: The Journal of Cell Biology

    Article Title: Vav3-induced cytoskeletal dynamics contribute to heterotypic properties of endothelial barriers

    doi: 10.1083/jcb.201706041

    Figure Lengend Snippet: High levels of barrier resistance correlate with continuous intercellular junctions and cortical arrangement of the actin cytoskeleton. (A) Confocal images of confluent endothelial monolayers displayed in order of low (HAEC, HBMVEC, and HUVEC) and high levels of barrier resistance (HLMVEC and HDMEC) left to right (bar, 20 µm; representative of n = 3). HLMVEC and HDMEC exhibit a linear and organized junctional staining of VE-cadherin, claudin-5, and ZO-1 compared with an irregular junctional pattern in cell types with lower levels of resistance. Phalloidin staining reveals a strict cortical arrangement of the actin cytoskeleton in HLMVEC and HDMEC, whereas cells with low resistance exhibit more stress fibers. Localization of cortactin is more peripheral and less cytoplasmic in HLMVECs and HDMECs. F-actin fibers aligned along the cell periphery, minimizing radial tension forces at cell junctions, indicated by linear junctional pattern of VE-cadherin/phalloidin overlay images (arrows) and lower presence of pMLC2 in HLMVECs and HDMECs. ( B–F) Graphs presenting mean values of fluorescence intensity across multiple cell–cell junctions per cell type (Fig. S2 B) for each barrier protein shown in A. Junctional components as well as phalloidin and cortactin are concentrated along the cell borders in HLMVECs and HDMECs compared with cell types with low barrier resistance.

    Article Snippet: Specifically, we obtained HUVECs (C2519A; Lonza; C-12203; PromoCell), HSaVECs (HSVEC/A; VEC-Technologies; cAP-0019; Angio-Proteomie), HAECs (PCS-100-011; ATCC; 6100; ScienCell), HIAECs (CC-2545; Lonza; cAP-0020; Angio-Proteomie), HBMVECs (ACBRI 376 V; Cell-Systems; cAP-0002; Angio-Proteomie), HUMVECs (C-12295; PromoCell; 7000; ScienCell), HLMVECs (3000; ScienCell; C-12281; PromoCell), HAMVECs (7200; ScienCell), and HDMECs (C-12212; PromoCell; 2000; ScienCell).

    Techniques: Staining, Fluorescence

    Knockdown of VAV3 reduces barrier strength and alters cytoskeletal arrangement in HDMECs and HLMVECs. (A) siRNA knockdown of three candidate genes with a strong correlation of expression to barrier resistance ( BAIAP2, VAV3, and SORBS2 ) validates the effect of VAV3 as an important regulator. (B) Efficiency of siRNA knockdown for BAIAP2, VAV3, and SORBS2 . (C and E) Effect of VAV3 silencing on barrier resistance compared with combined siRNA knockdown of VAV2 and VAV3 or CLDN5 (positive control) in HDMECs and HLMVECs. (D and F) Efficiency of siRNA knockdown for VAV2 , VAV3 , and CLDN5 (ECIS dataset C and E) in HDMECs and HLMVECs versus control siRNA. (G and H) Bar graphs of barrier resistance levels at 48 h for HDMECs and HLMVECs (ECIS dataset C and E). Error bars show mean ± SEM; *, P < 0.05; n = 3. (I) Table presenting ECIS data modeling values of R b , α , and C m at 48 h for HDMECs and HLMVECs with siRNA knockdown for VAV3 , VAV2/3 , and CLDN5 versus control siRNA, respectively (mean ± SEM; n = 3). (J) Immunofluorescence staining of VE-cadherin, ZO-1, F-actin (phalloidin), and cortactin in HDMEC monolayers subjected to either siRNA knockdown of VAV3 and VAV2/3 or siRNA control (bars, 20 µm). Magnification of phalloidin staining highlights loss of cortical actin and gain of stress fibers upon VAV3 and VAV2/3 knockdown. Translocation of cortactin to the cell periphery (filled arrows) is reduced in monolayers with siRNA knockdown of either VAV3 alone or VAV2/3 (open arrows). (K) Fluorescence intensity across cell–cell junctions (mean of n = 6) in cells exposed to siRNA control, siRNA VAV3 , and siRNA VAV2/3 (for VE-cadherin, ZO-1, phalloidin, and cortactin; as shown in J).

    Journal: The Journal of Cell Biology

    Article Title: Vav3-induced cytoskeletal dynamics contribute to heterotypic properties of endothelial barriers

    doi: 10.1083/jcb.201706041

    Figure Lengend Snippet: Knockdown of VAV3 reduces barrier strength and alters cytoskeletal arrangement in HDMECs and HLMVECs. (A) siRNA knockdown of three candidate genes with a strong correlation of expression to barrier resistance ( BAIAP2, VAV3, and SORBS2 ) validates the effect of VAV3 as an important regulator. (B) Efficiency of siRNA knockdown for BAIAP2, VAV3, and SORBS2 . (C and E) Effect of VAV3 silencing on barrier resistance compared with combined siRNA knockdown of VAV2 and VAV3 or CLDN5 (positive control) in HDMECs and HLMVECs. (D and F) Efficiency of siRNA knockdown for VAV2 , VAV3 , and CLDN5 (ECIS dataset C and E) in HDMECs and HLMVECs versus control siRNA. (G and H) Bar graphs of barrier resistance levels at 48 h for HDMECs and HLMVECs (ECIS dataset C and E). Error bars show mean ± SEM; *, P < 0.05; n = 3. (I) Table presenting ECIS data modeling values of R b , α , and C m at 48 h for HDMECs and HLMVECs with siRNA knockdown for VAV3 , VAV2/3 , and CLDN5 versus control siRNA, respectively (mean ± SEM; n = 3). (J) Immunofluorescence staining of VE-cadherin, ZO-1, F-actin (phalloidin), and cortactin in HDMEC monolayers subjected to either siRNA knockdown of VAV3 and VAV2/3 or siRNA control (bars, 20 µm). Magnification of phalloidin staining highlights loss of cortical actin and gain of stress fibers upon VAV3 and VAV2/3 knockdown. Translocation of cortactin to the cell periphery (filled arrows) is reduced in monolayers with siRNA knockdown of either VAV3 alone or VAV2/3 (open arrows). (K) Fluorescence intensity across cell–cell junctions (mean of n = 6) in cells exposed to siRNA control, siRNA VAV3 , and siRNA VAV2/3 (for VE-cadherin, ZO-1, phalloidin, and cortactin; as shown in J).

    Article Snippet: Specifically, we obtained HUVECs (C2519A; Lonza; C-12203; PromoCell), HSaVECs (HSVEC/A; VEC-Technologies; cAP-0019; Angio-Proteomie), HAECs (PCS-100-011; ATCC; 6100; ScienCell), HIAECs (CC-2545; Lonza; cAP-0020; Angio-Proteomie), HBMVECs (ACBRI 376 V; Cell-Systems; cAP-0002; Angio-Proteomie), HUMVECs (C-12295; PromoCell; 7000; ScienCell), HLMVECs (3000; ScienCell; C-12281; PromoCell), HAMVECs (7200; ScienCell), and HDMECs (C-12212; PromoCell; 2000; ScienCell).

    Techniques: Knockdown, Expressing, Positive Control, Control, Immunofluorescence, Staining, Translocation Assay, Fluorescence