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Cell Applications Inc human umbilical venous endothelial cells huvecs
Human Umbilical Venous Endothelial Cells Huvecs, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human umbilical venous endothelial cells huvecs/product/Cell Applications Inc
Average 86 stars, based on 1 article reviews
Price from $9.99 to $1999.99
human umbilical venous endothelial cells huvecs - by Bioz Stars, 2022-08
86/100 stars

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    Cell Applications Inc huvecs
    LINC00607 regulates basal EC and VSMC function. (A) Volcano plot indicating the DEGs upon 607-KD in <t>HUVECs.</t> Red and blue dots represent significantly up-regulated and down-regulated genes (with P -value cut-off of 0.01). Vertical dotted lines correspond to 2-fold differences. (B) Pathway enrichment analyses of DEGs upon 607-KD in HUVECs. Top 15 GO terms ranked by fold enrichment score for both the down- and up-regulated DEGs. (C) Expression of select down-regulated DEGs involved in angiogenesis due to LINC00607 knockdown (KD), as compared to scramble LNA (Scr). Heatmap is plotted based on z-scaled gene expression levels. (D) Representative images of tube formation of HUVEC transfected with either scramble or 607-KD at the indicated final concentration. The images were taken after incubating in Matrigel for 4 h. Scale bar = 100 μm. (E) Quantitative data of tube formation represented by numbers of tubes in randomly selected views. (F) DEGs upon 607-KD in VSMCs were plotted as in (A) . (G) Pathway enrichment analyses of DEGs upon 607-KD in VSMCs. Top 15 GO terms are plotted as in (B) . (H) Venn diagram showing the number of common DEGs upon 607-KD in HUVECs and VSMCs (in green). Numbers of unique DEGs in each cell type (pink for HUVECs and blue for VSMCs) are indicated. (I) Polygon radar chart showing the top 5 enriched pathways of the common DEGs in HUVECs and VSMCs. Data values for each vertex represent the number of DEGs classified in the indicated gene pathway in blue and the P -value (in -log 10 ) in orange. (J) Expression heatmap of representative DEGs commonly affected by 607-KD in ECs and VSMCs.
    Huvecs, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/huvecs/product/Cell Applications Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    huvecs - by Bioz Stars, 2022-08
    86/100 stars
      Buy from Supplier

    86
    Cell Applications Inc hdl huvecs
    <t>HDL</t> attenuates dextrose-induced inhibition of ERK activation. <t>HUVECs</t> were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ), or HDL (5–120 µg/mL) ( b ), *p
    Hdl Huvecs, supplied by Cell Applications Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/hdl huvecs/product/Cell Applications Inc
    Average 86 stars, based on 1 article reviews
    Price from $9.99 to $1999.99
    hdl huvecs - by Bioz Stars, 2022-08
    86/100 stars
      Buy from Supplier

    Image Search Results


    LINC00607 regulates basal EC and VSMC function. (A) Volcano plot indicating the DEGs upon 607-KD in HUVECs. Red and blue dots represent significantly up-regulated and down-regulated genes (with P -value cut-off of 0.01). Vertical dotted lines correspond to 2-fold differences. (B) Pathway enrichment analyses of DEGs upon 607-KD in HUVECs. Top 15 GO terms ranked by fold enrichment score for both the down- and up-regulated DEGs. (C) Expression of select down-regulated DEGs involved in angiogenesis due to LINC00607 knockdown (KD), as compared to scramble LNA (Scr). Heatmap is plotted based on z-scaled gene expression levels. (D) Representative images of tube formation of HUVEC transfected with either scramble or 607-KD at the indicated final concentration. The images were taken after incubating in Matrigel for 4 h. Scale bar = 100 μm. (E) Quantitative data of tube formation represented by numbers of tubes in randomly selected views. (F) DEGs upon 607-KD in VSMCs were plotted as in (A) . (G) Pathway enrichment analyses of DEGs upon 607-KD in VSMCs. Top 15 GO terms are plotted as in (B) . (H) Venn diagram showing the number of common DEGs upon 607-KD in HUVECs and VSMCs (in green). Numbers of unique DEGs in each cell type (pink for HUVECs and blue for VSMCs) are indicated. (I) Polygon radar chart showing the top 5 enriched pathways of the common DEGs in HUVECs and VSMCs. Data values for each vertex represent the number of DEGs classified in the indicated gene pathway in blue and the P -value (in -log 10 ) in orange. (J) Expression heatmap of representative DEGs commonly affected by 607-KD in ECs and VSMCs.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Vascular Regulation by Super Enhancer-Derived LINC00607

    doi: 10.3389/fcvm.2022.881916

    Figure Lengend Snippet: LINC00607 regulates basal EC and VSMC function. (A) Volcano plot indicating the DEGs upon 607-KD in HUVECs. Red and blue dots represent significantly up-regulated and down-regulated genes (with P -value cut-off of 0.01). Vertical dotted lines correspond to 2-fold differences. (B) Pathway enrichment analyses of DEGs upon 607-KD in HUVECs. Top 15 GO terms ranked by fold enrichment score for both the down- and up-regulated DEGs. (C) Expression of select down-regulated DEGs involved in angiogenesis due to LINC00607 knockdown (KD), as compared to scramble LNA (Scr). Heatmap is plotted based on z-scaled gene expression levels. (D) Representative images of tube formation of HUVEC transfected with either scramble or 607-KD at the indicated final concentration. The images were taken after incubating in Matrigel for 4 h. Scale bar = 100 μm. (E) Quantitative data of tube formation represented by numbers of tubes in randomly selected views. (F) DEGs upon 607-KD in VSMCs were plotted as in (A) . (G) Pathway enrichment analyses of DEGs upon 607-KD in VSMCs. Top 15 GO terms are plotted as in (B) . (H) Venn diagram showing the number of common DEGs upon 607-KD in HUVECs and VSMCs (in green). Numbers of unique DEGs in each cell type (pink for HUVECs and blue for VSMCs) are indicated. (I) Polygon radar chart showing the top 5 enriched pathways of the common DEGs in HUVECs and VSMCs. Data values for each vertex represent the number of DEGs classified in the indicated gene pathway in blue and the P -value (in -log 10 ) in orange. (J) Expression heatmap of representative DEGs commonly affected by 607-KD in ECs and VSMCs.

    Article Snippet: For most in vitro experiments involving ECs, human umbilical vein ECs, i.e., HUVECs (Cell Applications Inc., San Diego, CA, Catalog # 200p-05n and lot # 3,363 and 2,914) between passages 5–8 pooled from multiple donors were used after testing negative for mycoplasma contamination.

    Techniques: Expressing, Transfection, Concentration Assay

    Stimulus-dependent regulatory function of LINC00607 in ECs. (A) Representative images of smFISH detecting LINC00607 (green) in HUVEC treated with normal glucose (5.5 mM D-glucose) and osmolarity control (NM) or 25 mM D-glucose and 5 ng/ml TNFα (HT) for 3 days. DAPI staining indicates the nuclei. Scale bar = 20 μm. (B) Quantitative data of LINC00607 signal per nucleus. LINC00607 signal from 18 nuclei for NM and 24 nuclei for HT was quantified using ImageJ. (C) Venn diagram showing the number of common DEGs in HUVECs upon 607-KD under basal and HT conditions (green). Numbers of unique DEGs in each condition (pink for NM and blue for HT) are indicated. (D) Expression pattern of select DEGs commonly regulated by 607-KD in HUVECs under both baseline and HT. Heatmap is plotted based on z-scaled average gene expression levels. (E) Putative sequence of c-Myc binding site at the LINC00607 promoters (Chr2: 215826423-215837423, Chr2: 215830609-215841609, and Chr2: 215842628-215853628) predicted by TRANSFAC. The HUVEC c-Myc ChIP-seq tracks (ENCODE data ENCFF000RUU) at LINC00607 (green), SERPINE1 (red), and APEX1 (purple) genomic loci were plotted using Epigenome Browser. CAGE tracks indicating the putative alternative TSS for LINC00607 is shown in blue (F) Network map showing MYC as a top candidate TF for LINC00607-regulated DEGs. The relationship between MYC and downstream targets are displayed as edges between nodes. The color intensity of each node represents fold change expression, red (upregulated), and green (downregulated). The edges denote predicted relationships with orange indicating activation, blue indicating inhibition and gray representing an unpredicted effect. (G,H) qPCR analysis of indicated transcripts in HUVECs transfected with respective siRNAs under basal condition (G) or HT (H) . The respective scramble control was set as 1. Data represents mean ± SEM from 3 independent experiments. * P

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Vascular Regulation by Super Enhancer-Derived LINC00607

    doi: 10.3389/fcvm.2022.881916

    Figure Lengend Snippet: Stimulus-dependent regulatory function of LINC00607 in ECs. (A) Representative images of smFISH detecting LINC00607 (green) in HUVEC treated with normal glucose (5.5 mM D-glucose) and osmolarity control (NM) or 25 mM D-glucose and 5 ng/ml TNFα (HT) for 3 days. DAPI staining indicates the nuclei. Scale bar = 20 μm. (B) Quantitative data of LINC00607 signal per nucleus. LINC00607 signal from 18 nuclei for NM and 24 nuclei for HT was quantified using ImageJ. (C) Venn diagram showing the number of common DEGs in HUVECs upon 607-KD under basal and HT conditions (green). Numbers of unique DEGs in each condition (pink for NM and blue for HT) are indicated. (D) Expression pattern of select DEGs commonly regulated by 607-KD in HUVECs under both baseline and HT. Heatmap is plotted based on z-scaled average gene expression levels. (E) Putative sequence of c-Myc binding site at the LINC00607 promoters (Chr2: 215826423-215837423, Chr2: 215830609-215841609, and Chr2: 215842628-215853628) predicted by TRANSFAC. The HUVEC c-Myc ChIP-seq tracks (ENCODE data ENCFF000RUU) at LINC00607 (green), SERPINE1 (red), and APEX1 (purple) genomic loci were plotted using Epigenome Browser. CAGE tracks indicating the putative alternative TSS for LINC00607 is shown in blue (F) Network map showing MYC as a top candidate TF for LINC00607-regulated DEGs. The relationship between MYC and downstream targets are displayed as edges between nodes. The color intensity of each node represents fold change expression, red (upregulated), and green (downregulated). The edges denote predicted relationships with orange indicating activation, blue indicating inhibition and gray representing an unpredicted effect. (G,H) qPCR analysis of indicated transcripts in HUVECs transfected with respective siRNAs under basal condition (G) or HT (H) . The respective scramble control was set as 1. Data represents mean ± SEM from 3 independent experiments. * P

    Article Snippet: For most in vitro experiments involving ECs, human umbilical vein ECs, i.e., HUVECs (Cell Applications Inc., San Diego, CA, Catalog # 200p-05n and lot # 3,363 and 2,914) between passages 5–8 pooled from multiple donors were used after testing negative for mycoplasma contamination.

    Techniques: Staining, Expressing, Sequencing, Binding Assay, Chromatin Immunoprecipitation, Activation Assay, Inhibition, Real-time Polymerase Chain Reaction, Transfection

    LINC00607 inhibition reverses the effect of HT in ECs. (A) Experimental design of HT to NM switch experiment. HUVECs were treated with NM or HT for 3 days, and then switched to NM medium for another 1 (H3N1) or 3 days (H3N3) before cell harvest. (B) qPCR detection of FN1 mRNA levels from experiment shown as in (A) . (C) Experimental design of the “reverse” experiment. HUVECs in biological replicates were treated with NM or HT for 7 days, or HT for 4 days before LINC00607 knockdown using LNA GapmeR (607-KD). (D) LINC00607 expression quantified by scRNA-seq of three groups of ECs. (E–H) Representative reversible ( FN1 and SERPINE1 ) and irreversible ( CCL2 and SMAD3 ) DEGs. (I) UMAP of HT-KD scRNA-seq data. (J) LINC00607 expression in HT-KD samples shown on UMAP separated by 7 clusters. Note that Cluster 0, 1, and 6 show high LINC00607 levels (expression level > 1, i.e., 607-Hi cells) and Cluster 4 shows the lowest LINC00607 level (i.e., 607-Lo cells). (K) LINC00607 expression in 7 clusters of cells in HT-KD samples plotted by UMAP. (L–N) Representative DEGs in HT-KD samples plotted on UMAP. (O) Heatmap showing the expression of indicated DEGs in LINC00607-Lo vs. -Hi ECs.

    Journal: Frontiers in Cardiovascular Medicine

    Article Title: Vascular Regulation by Super Enhancer-Derived LINC00607

    doi: 10.3389/fcvm.2022.881916

    Figure Lengend Snippet: LINC00607 inhibition reverses the effect of HT in ECs. (A) Experimental design of HT to NM switch experiment. HUVECs were treated with NM or HT for 3 days, and then switched to NM medium for another 1 (H3N1) or 3 days (H3N3) before cell harvest. (B) qPCR detection of FN1 mRNA levels from experiment shown as in (A) . (C) Experimental design of the “reverse” experiment. HUVECs in biological replicates were treated with NM or HT for 7 days, or HT for 4 days before LINC00607 knockdown using LNA GapmeR (607-KD). (D) LINC00607 expression quantified by scRNA-seq of three groups of ECs. (E–H) Representative reversible ( FN1 and SERPINE1 ) and irreversible ( CCL2 and SMAD3 ) DEGs. (I) UMAP of HT-KD scRNA-seq data. (J) LINC00607 expression in HT-KD samples shown on UMAP separated by 7 clusters. Note that Cluster 0, 1, and 6 show high LINC00607 levels (expression level > 1, i.e., 607-Hi cells) and Cluster 4 shows the lowest LINC00607 level (i.e., 607-Lo cells). (K) LINC00607 expression in 7 clusters of cells in HT-KD samples plotted by UMAP. (L–N) Representative DEGs in HT-KD samples plotted on UMAP. (O) Heatmap showing the expression of indicated DEGs in LINC00607-Lo vs. -Hi ECs.

    Article Snippet: For most in vitro experiments involving ECs, human umbilical vein ECs, i.e., HUVECs (Cell Applications Inc., San Diego, CA, Catalog # 200p-05n and lot # 3,363 and 2,914) between passages 5–8 pooled from multiple donors were used after testing negative for mycoplasma contamination.

    Techniques: Inhibition, Real-time Polymerase Chain Reaction, Expressing

    Mincle colocalizes with added fluorescent GSLs in human endothelial cells. ( Left ) Three-dimensional SIM in HUVECs. HUVECs were incubated for 1 h with exogenously added fluorescent GSLs, washed, fixed, labeled with antibodies against Mincle, and analyzed by SIM. Glucosylceramide and lactosylceramide fluorescently labeled with NBD and ganglioside GM3 fluorescently labeled with TopFluor were used. Fluorescent glycoshingolipids are pseudocolored in green and Mincle in red; colocalization is indicated by yellow pseudocoloring. Representative cells are shown. Two independent experiments were performed. ( Right ) Statistical analyses of GSL/Mincle colocalization using the Pearson correlation coefficient; n = 15 independent fields per quantification. The results are presented as the mean ± SD values.

    Journal: Proceedings of the National Academy of Sciences of the United States of America

    Article Title: A mechanism of self-lipid endocytosis mediated by the receptor Mincle

    doi: 10.1073/pnas.2120489119

    Figure Lengend Snippet: Mincle colocalizes with added fluorescent GSLs in human endothelial cells. ( Left ) Three-dimensional SIM in HUVECs. HUVECs were incubated for 1 h with exogenously added fluorescent GSLs, washed, fixed, labeled with antibodies against Mincle, and analyzed by SIM. Glucosylceramide and lactosylceramide fluorescently labeled with NBD and ganglioside GM3 fluorescently labeled with TopFluor were used. Fluorescent glycoshingolipids are pseudocolored in green and Mincle in red; colocalization is indicated by yellow pseudocoloring. Representative cells are shown. Two independent experiments were performed. ( Right ) Statistical analyses of GSL/Mincle colocalization using the Pearson correlation coefficient; n = 15 independent fields per quantification. The results are presented as the mean ± SD values.

    Article Snippet: HUVECs were purchased from Cell Applications Inc. For colocalization analysis we used the Coloc2 Plugin in Fiji ( ) to calculate the Pearson correlation coefficient after threshold adjustment via the Costes method ( ).

    Techniques: Incubation, Labeling

    Successful engraftment of generated hPSC-derived EPs to form functional vessels in vivo . (A) Schematic of our finalized approach for generation of hPSC-derived EPs (VEC + CD31 + CD34 + CD14 − ). This is comprised of phase 1 and 2 in only 6 days, and sequential application of the following molecules: BMP4/GSK-3βI in phase 1 and VEGF-A/DAPT in phase 2. (B) Comparison of cell numbers of hPSCs before differentiation, generated EPs (day 6), and VEC + CD31 + ECs (day 14) after phase 3 expansion using our differentiation protocol. (C) Matrigel (MG) plugs with hPSC-derived EPs subcutaneously transplanted into NOD/SCID mice. In vivo live images of capillary vessel formation generated by the hPSC-derived VEC-EGFP + EPs 2 weeks after transplantation. BF, bright field. Scale bars, 100 μm (bottom) and 200 μm (top). (D) The MG plug with hPSC-derived EPs were harvested 4 weeks after transplantation (top), fixed in 2% paraformaldehyde (bottom, left), and subjected to fluorescent whole-mount immunostaining. The bottom-right panel shows anastomosis (arrowhead) between the neovessel formed by transplanted EGFP + EPs and a host vessel of NOD/SCID mice expressing murine VE-cadherin (red). Scale bars, 500 μm (top) and 200 μm (bottom, right). (E) Fluorescent immunostaining of cryosections of the MG plug in D shows anastomoses (arrowheads) between the neovessel formed by transplanted EGFP + EPs and host capillary vessels of NOD/SCID mice expressing murine VE-cadherin (red). Scale bar, 20 μm. (F) The neovessels formed by transplanted EGFP + EPs in a Matrigel plug with functional anastomosis (arrowhead) to native vessels were labeled with lectin (GS-IB 4 , blue). Scale bar, 20 μm. (G) In vivo live images of EGFP + EP-derived capillary vessels 3 months after transplantation. Black arrowheads indicate host angiogenic sprouting capillary vessels, whereas white arrowheads indicate neovessels formed by transplanted EPs in connection with host sprouting vessels. Scale bars, 100 μm. (H) The transplanted cell numbers of EPs (VEC + CD31 + CD34 + CD14 − ) sorted on day 6, ECs (VEC + CD31 + ) sorted on day 14 or VEC-EGFP + HUVECs were positively correlated with quantitative total tube area in in vivo Matrigel plugs. EPs have a three- to fivefold efficacy of quantitative vascular tube formation in vivo , compared with ECs or HUVECs. * P

    Journal: Cell Research

    Article Title: Manipulation of a VEGF-Notch signaling circuit drives formation of functional vascular endothelial progenitors from human pluripotent stem cells

    doi: 10.1038/cr.2014.59

    Figure Lengend Snippet: Successful engraftment of generated hPSC-derived EPs to form functional vessels in vivo . (A) Schematic of our finalized approach for generation of hPSC-derived EPs (VEC + CD31 + CD34 + CD14 − ). This is comprised of phase 1 and 2 in only 6 days, and sequential application of the following molecules: BMP4/GSK-3βI in phase 1 and VEGF-A/DAPT in phase 2. (B) Comparison of cell numbers of hPSCs before differentiation, generated EPs (day 6), and VEC + CD31 + ECs (day 14) after phase 3 expansion using our differentiation protocol. (C) Matrigel (MG) plugs with hPSC-derived EPs subcutaneously transplanted into NOD/SCID mice. In vivo live images of capillary vessel formation generated by the hPSC-derived VEC-EGFP + EPs 2 weeks after transplantation. BF, bright field. Scale bars, 100 μm (bottom) and 200 μm (top). (D) The MG plug with hPSC-derived EPs were harvested 4 weeks after transplantation (top), fixed in 2% paraformaldehyde (bottom, left), and subjected to fluorescent whole-mount immunostaining. The bottom-right panel shows anastomosis (arrowhead) between the neovessel formed by transplanted EGFP + EPs and a host vessel of NOD/SCID mice expressing murine VE-cadherin (red). Scale bars, 500 μm (top) and 200 μm (bottom, right). (E) Fluorescent immunostaining of cryosections of the MG plug in D shows anastomoses (arrowheads) between the neovessel formed by transplanted EGFP + EPs and host capillary vessels of NOD/SCID mice expressing murine VE-cadherin (red). Scale bar, 20 μm. (F) The neovessels formed by transplanted EGFP + EPs in a Matrigel plug with functional anastomosis (arrowhead) to native vessels were labeled with lectin (GS-IB 4 , blue). Scale bar, 20 μm. (G) In vivo live images of EGFP + EP-derived capillary vessels 3 months after transplantation. Black arrowheads indicate host angiogenic sprouting capillary vessels, whereas white arrowheads indicate neovessels formed by transplanted EPs in connection with host sprouting vessels. Scale bars, 100 μm. (H) The transplanted cell numbers of EPs (VEC + CD31 + CD34 + CD14 − ) sorted on day 6, ECs (VEC + CD31 + ) sorted on day 14 or VEC-EGFP + HUVECs were positively correlated with quantitative total tube area in in vivo Matrigel plugs. EPs have a three- to fivefold efficacy of quantitative vascular tube formation in vivo , compared with ECs or HUVECs. * P

    Article Snippet: In vitro vascular tube formation assay 50 μl Matrigel per well was placed into wells of a 96-well plate and incubated at 37 °C for 1 h. 1.5 × 104 of either hPSC-derived endothelial lineage cells sorted by FACS, HUVECs (Cell Applications Inc) or HUCBCs (Harvard University) were suspended in 100 μl of EBM-2 supplemented with 5% FBS and 50 ng/ml VEGF, and then seeded onto the Matrigel plugs.

    Techniques: Generated, Derivative Assay, Functional Assay, In Vivo, Mouse Assay, Transplantation Assay, Immunostaining, Expressing, Labeling

    HDL attenuates dextrose-induced inhibition of ERK activation. HUVECs were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ), or HDL (5–120 µg/mL) ( b ), *p

    Journal: Cardiovascular Diabetology

    Article Title: High-density lipoproteins attenuate high glucose-impaired endothelial cell signaling and functions: potential implications for improved vascular repair in diabetes

    doi: 10.1186/s12933-017-0605-8

    Figure Lengend Snippet: HDL attenuates dextrose-induced inhibition of ERK activation. HUVECs were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ), or HDL (5–120 µg/mL) ( b ), *p

    Article Snippet: Cell isolation, culture and preparation of HDL HUVECs (Cell Applications Inc., San Diego, CA, USA) were maintained in MCDB (Molecular, Cellular, and Developmental Biology) medium containing 15% fetal bovine serum (FBS, lipoprotein deficient), 0.009% heparin, 0.015% endothelial cell growth supplement (Cat.

    Techniques: Inhibition, Activation Assay, Incubation

    HDL attenuates dextrose-induced inhibition of p38 activation. HUVECs were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ) or HDL (5–120 µg/mL) ( b ), *p

    Journal: Cardiovascular Diabetology

    Article Title: High-density lipoproteins attenuate high glucose-impaired endothelial cell signaling and functions: potential implications for improved vascular repair in diabetes

    doi: 10.1186/s12933-017-0605-8

    Figure Lengend Snippet: HDL attenuates dextrose-induced inhibition of p38 activation. HUVECs were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ) or HDL (5–120 µg/mL) ( b ), *p

    Article Snippet: Cell isolation, culture and preparation of HDL HUVECs (Cell Applications Inc., San Diego, CA, USA) were maintained in MCDB (Molecular, Cellular, and Developmental Biology) medium containing 15% fetal bovine serum (FBS, lipoprotein deficient), 0.009% heparin, 0.015% endothelial cell growth supplement (Cat.

    Techniques: Inhibition, Activation Assay, Incubation

    HDL rescues dextrose-induced inhibition of HUVEC migration. HUVEC migration was determined using transwell membranes. HUVECs were seeded on the upper chamber, serum-deprived for 12 h, then the transwells were placed into the lower chamber containing increasing dextrose concentrations (5.7–40 mM) and/or HDL (80 μg/mL) and incubated overnight. The cells that migrated through the membrane were fixed and stained by DAPI. Upper panels are representative images of membranes of migrated cells. Data shown are the mean ± SEM of results performed in triplicate from 3 independent experiments. # p

    Journal: Cardiovascular Diabetology

    Article Title: High-density lipoproteins attenuate high glucose-impaired endothelial cell signaling and functions: potential implications for improved vascular repair in diabetes

    doi: 10.1186/s12933-017-0605-8

    Figure Lengend Snippet: HDL rescues dextrose-induced inhibition of HUVEC migration. HUVEC migration was determined using transwell membranes. HUVECs were seeded on the upper chamber, serum-deprived for 12 h, then the transwells were placed into the lower chamber containing increasing dextrose concentrations (5.7–40 mM) and/or HDL (80 μg/mL) and incubated overnight. The cells that migrated through the membrane were fixed and stained by DAPI. Upper panels are representative images of membranes of migrated cells. Data shown are the mean ± SEM of results performed in triplicate from 3 independent experiments. # p

    Article Snippet: Cell isolation, culture and preparation of HDL HUVECs (Cell Applications Inc., San Diego, CA, USA) were maintained in MCDB (Molecular, Cellular, and Developmental Biology) medium containing 15% fetal bovine serum (FBS, lipoprotein deficient), 0.009% heparin, 0.015% endothelial cell growth supplement (Cat.

    Techniques: Inhibition, Migration, Incubation, Staining

    HDL attenuates dextrose-induced inhibition of HUVEC proliferation. a Cell proliferation was determined after cells were incubated with dextrose (5.7, 20 and 40 mM) or dextrose plus HDL (80 µg/mL) for 96 h using BrdU incorporation. 2.5% FBS (control) and 15% FBS (positive control) treatments were also included. b Protein levels of PCNA were determined in HUVEC lysates incubated with dextrose (5.7, 20 and 40 mM) or dextrose plus HDL (80 µg/mL) for 72 h using Western blotting. β-Actin was used as the protein loading control. Data shown are the mean ± SEM of results from three independent experiments. # p

    Journal: Cardiovascular Diabetology

    Article Title: High-density lipoproteins attenuate high glucose-impaired endothelial cell signaling and functions: potential implications for improved vascular repair in diabetes

    doi: 10.1186/s12933-017-0605-8

    Figure Lengend Snippet: HDL attenuates dextrose-induced inhibition of HUVEC proliferation. a Cell proliferation was determined after cells were incubated with dextrose (5.7, 20 and 40 mM) or dextrose plus HDL (80 µg/mL) for 96 h using BrdU incorporation. 2.5% FBS (control) and 15% FBS (positive control) treatments were also included. b Protein levels of PCNA were determined in HUVEC lysates incubated with dextrose (5.7, 20 and 40 mM) or dextrose plus HDL (80 µg/mL) for 72 h using Western blotting. β-Actin was used as the protein loading control. Data shown are the mean ± SEM of results from three independent experiments. # p

    Article Snippet: Cell isolation, culture and preparation of HDL HUVECs (Cell Applications Inc., San Diego, CA, USA) were maintained in MCDB (Molecular, Cellular, and Developmental Biology) medium containing 15% fetal bovine serum (FBS, lipoprotein deficient), 0.009% heparin, 0.015% endothelial cell growth supplement (Cat.

    Techniques: Inhibition, Incubation, BrdU Incorporation Assay, Positive Control, Western Blot

    HDL mitigates the inhibition of Akt phosphorylation by dextrose. HUVECs were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ) or HDL (5–120 µg/mL) ( b ), *p

    Journal: Cardiovascular Diabetology

    Article Title: High-density lipoproteins attenuate high glucose-impaired endothelial cell signaling and functions: potential implications for improved vascular repair in diabetes

    doi: 10.1186/s12933-017-0605-8

    Figure Lengend Snippet: HDL mitigates the inhibition of Akt phosphorylation by dextrose. HUVECs were incubated with increasing dextrose concentrations (5.7–60 mM) for 15 min ( a ) or HDL (5–120 µg/mL) ( b ), *p

    Article Snippet: Cell isolation, culture and preparation of HDL HUVECs (Cell Applications Inc., San Diego, CA, USA) were maintained in MCDB (Molecular, Cellular, and Developmental Biology) medium containing 15% fetal bovine serum (FBS, lipoprotein deficient), 0.009% heparin, 0.015% endothelial cell growth supplement (Cat.

    Techniques: Inhibition, Incubation