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primary human coronary artery endothelial cells hcaecs  (PromoCell)


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    PromoCell primary human coronary artery endothelial cells hcaecs
    Primary Human Coronary Artery Endothelial Cells Hcaecs, supplied by PromoCell, used in various techniques. Bioz Stars score: 96/100, based on 228 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/artery+endothelial+cells/Human+Coronary+Artery+Endothelial+Cells/pm42259138-95-0-11
    Average 96 stars, based on 228 article reviews
    primary human coronary artery endothelial cells hcaecs - by Bioz Stars, 2026-09
    96/100 stars

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    Cell Culture:

    Article Title: Functionality of Endothelial Cells and Pericytes From Human Pluripotent Stem Cells Demonstrated in Cultured Vascular Plexus and Zebrafish Xenografts
    Article Snippet: .. Primary human umbilical vein and artery endothelial cells (HUVEC and HUAEC respectively) were purchased from PromoCell and cultured as previously described5. .. Purification of ECs was carried out on day 10 of differentiation with the CD31-labeled Dynabeads (Life Technologies, 1115D), as previously described6,7.



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    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected <t>HCAECs</t> was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.
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    Multiplexed ELISA of conditioned media from unstimulated umbilical artery (HUAEC), umbilical vein (HUVEC), dermal microvascular (HDMEC), and pulmonary microvascular (HPMEC) endothelial cells. Conditioned media was collected from 1 well per cell type after 16 hours incubation. Samples were analyzed with a Luminex Magpix device and a custom ProcartaPlex inflammation panel. Data are represented as (A) Heatmap normalized across the range for each protein, with darker tones corresponding to higher expression and less expression for lighter tones. Factors that measured below the limit of detection are indicated with an X. (B) log 10 (average expression) ± SEM for N=4 independent experiments. Factors that measured below the limit of detection are indicated with an X. Full statistical analysis with one-way ANOVA and Tukey-Kramer pairwise comparisons testing was done for average expression across all cell types, with results presented in Supplemental Figure 1.

    Journal: bioRxiv

    Article Title: Endothelial Heterogeneity Across Vascular Beds Impacts Inflammatory Signaling and Neutrophil Adhesion

    doi: 10.64898/2026.05.26.727909

    Figure Lengend Snippet: Multiplexed ELISA of conditioned media from unstimulated umbilical artery (HUAEC), umbilical vein (HUVEC), dermal microvascular (HDMEC), and pulmonary microvascular (HPMEC) endothelial cells. Conditioned media was collected from 1 well per cell type after 16 hours incubation. Samples were analyzed with a Luminex Magpix device and a custom ProcartaPlex inflammation panel. Data are represented as (A) Heatmap normalized across the range for each protein, with darker tones corresponding to higher expression and less expression for lighter tones. Factors that measured below the limit of detection are indicated with an X. (B) log 10 (average expression) ± SEM for N=4 independent experiments. Factors that measured below the limit of detection are indicated with an X. Full statistical analysis with one-way ANOVA and Tukey-Kramer pairwise comparisons testing was done for average expression across all cell types, with results presented in Supplemental Figure 1.

    Article Snippet: The following cells were used: pooled human umbilical vein endothelial cells (HUVEC, PromoCell C-12203, Heidelberg, Germany), human umbilical arterial endothelial cells (HUAEC, PromoCell C-12202, Heidelberg, Germany), adult dermal microvascular endothelial cells (HDMEC, PromoCell C-12212, Heidelberg, Germany), and adult pulmonary microvascular endothelial cells (HPMEC, PromoCell C-12281, Heidelberg, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Incubation, Luminex, Expressing

    Multiplexed ELISA of conditioned media from TNF-stimulated (50ng/mL TNF in media) umbilical artery (HUAEC), umbilical vein (HUVEC), dermal microvascular (HDMEC), and pulmonary microvascular (HPMEC) endothelial cells. Conditioned media was collected from 1 well per cell type after 16 hours incubation. Samples were analyzed with a Luminex Magpix device and a custom ProcartaPlex inflammation panel. (A) Heatmap normalized across the range for each protein, with darker tones corresponding to higher expression and less expression for lighter tones. (B) Fold-change expression differences from unstimulated control for factors with >8 fold increase by at least one cell type. Data are average fold change-expression for N=4 independent experiments. One-way ANOVA with Tukey-Kramer pairwise comparisons testing was done for each condition, with asterisks indicating statistical significance between conditions (*p<0.05).

    Journal: bioRxiv

    Article Title: Endothelial Heterogeneity Across Vascular Beds Impacts Inflammatory Signaling and Neutrophil Adhesion

    doi: 10.64898/2026.05.26.727909

    Figure Lengend Snippet: Multiplexed ELISA of conditioned media from TNF-stimulated (50ng/mL TNF in media) umbilical artery (HUAEC), umbilical vein (HUVEC), dermal microvascular (HDMEC), and pulmonary microvascular (HPMEC) endothelial cells. Conditioned media was collected from 1 well per cell type after 16 hours incubation. Samples were analyzed with a Luminex Magpix device and a custom ProcartaPlex inflammation panel. (A) Heatmap normalized across the range for each protein, with darker tones corresponding to higher expression and less expression for lighter tones. (B) Fold-change expression differences from unstimulated control for factors with >8 fold increase by at least one cell type. Data are average fold change-expression for N=4 independent experiments. One-way ANOVA with Tukey-Kramer pairwise comparisons testing was done for each condition, with asterisks indicating statistical significance between conditions (*p<0.05).

    Article Snippet: The following cells were used: pooled human umbilical vein endothelial cells (HUVEC, PromoCell C-12203, Heidelberg, Germany), human umbilical arterial endothelial cells (HUAEC, PromoCell C-12202, Heidelberg, Germany), adult dermal microvascular endothelial cells (HDMEC, PromoCell C-12212, Heidelberg, Germany), and adult pulmonary microvascular endothelial cells (HPMEC, PromoCell C-12281, Heidelberg, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Incubation, Luminex, Expressing, Control

    Multiplexed ELISA of conditioned media from P. aeuriginosa -stimulated (0.05 OD in media) umbilical artery (HUAEC), umbilical vein (HUVEC), dermal microvascular (HDMEC), and pulmonary microvascular (HPMEC) endothelial cells. Conditioned media was collected from 1 well per cell type after 16 hours incubation. Samples were analyzed with a Luminex Magpix device and a custom ProcartaPlex inflammation panel. (A) Heatmap normalized across the range for each protein, with darker tones corresponding to higher expression and less expression for lighter tones. (B) Fold-change expression differences from unstimulated control for factors with >8 fold increase by at least one cell type. Data are average fold change-expression for N=4 independent experiments. One-way ANOVA with Tukey-Kramer pairwise comparisons testing was done for each condition, with asterisks indicating statistical significance between conditions (*p<0.05).

    Journal: bioRxiv

    Article Title: Endothelial Heterogeneity Across Vascular Beds Impacts Inflammatory Signaling and Neutrophil Adhesion

    doi: 10.64898/2026.05.26.727909

    Figure Lengend Snippet: Multiplexed ELISA of conditioned media from P. aeuriginosa -stimulated (0.05 OD in media) umbilical artery (HUAEC), umbilical vein (HUVEC), dermal microvascular (HDMEC), and pulmonary microvascular (HPMEC) endothelial cells. Conditioned media was collected from 1 well per cell type after 16 hours incubation. Samples were analyzed with a Luminex Magpix device and a custom ProcartaPlex inflammation panel. (A) Heatmap normalized across the range for each protein, with darker tones corresponding to higher expression and less expression for lighter tones. (B) Fold-change expression differences from unstimulated control for factors with >8 fold increase by at least one cell type. Data are average fold change-expression for N=4 independent experiments. One-way ANOVA with Tukey-Kramer pairwise comparisons testing was done for each condition, with asterisks indicating statistical significance between conditions (*p<0.05).

    Article Snippet: The following cells were used: pooled human umbilical vein endothelial cells (HUVEC, PromoCell C-12203, Heidelberg, Germany), human umbilical arterial endothelial cells (HUAEC, PromoCell C-12202, Heidelberg, Germany), adult dermal microvascular endothelial cells (HDMEC, PromoCell C-12212, Heidelberg, Germany), and adult pulmonary microvascular endothelial cells (HPMEC, PromoCell C-12281, Heidelberg, Germany).

    Techniques: Enzyme-linked Immunosorbent Assay, Incubation, Luminex, Expressing, Control

    Endothelial cells were cultured in 96-well plates and activated with control, TNF(50 ng/mL) or P. aeruginosa (0.05 OD) media for 2 hours. Neutrophils isolated from whole blood were added to each well and incubated for 15 minutes, then imaged before and after 5x PBS washes. (A) Representative images of endothelial cells (red) and neutrophils (green) before and after washing to remove non-adherent cells. (Scale bar = 100 μm) (B, C) Neutrophil adhesion fraction was quantified by counting neutrophils adherent after washing and dividing by the neutrophil count before washing. Data represent average adhesion fraction ± SEM for 3 independent experiments per cell type. One-way ANOVA with Tukey-Kramer pairwise comparisons testing was done for each condition, with asterisks indicating statistical significance between conditions (*p<0.05).

    Journal: bioRxiv

    Article Title: Endothelial Heterogeneity Across Vascular Beds Impacts Inflammatory Signaling and Neutrophil Adhesion

    doi: 10.64898/2026.05.26.727909

    Figure Lengend Snippet: Endothelial cells were cultured in 96-well plates and activated with control, TNF(50 ng/mL) or P. aeruginosa (0.05 OD) media for 2 hours. Neutrophils isolated from whole blood were added to each well and incubated for 15 minutes, then imaged before and after 5x PBS washes. (A) Representative images of endothelial cells (red) and neutrophils (green) before and after washing to remove non-adherent cells. (Scale bar = 100 μm) (B, C) Neutrophil adhesion fraction was quantified by counting neutrophils adherent after washing and dividing by the neutrophil count before washing. Data represent average adhesion fraction ± SEM for 3 independent experiments per cell type. One-way ANOVA with Tukey-Kramer pairwise comparisons testing was done for each condition, with asterisks indicating statistical significance between conditions (*p<0.05).

    Article Snippet: The following cells were used: pooled human umbilical vein endothelial cells (HUVEC, PromoCell C-12203, Heidelberg, Germany), human umbilical arterial endothelial cells (HUAEC, PromoCell C-12202, Heidelberg, Germany), adult dermal microvascular endothelial cells (HDMEC, PromoCell C-12212, Heidelberg, Germany), and adult pulmonary microvascular endothelial cells (HPMEC, PromoCell C-12281, Heidelberg, Germany).

    Techniques: Cell Culture, Control, Isolation, Incubation

    MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected HCAECs was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MRMP mediates upregulation of MPC1. (A) MPC1 mRNA expression in MRMP-infected HCAECs was determined using qRT-PCR ( n = 3). (B,C) MPC1 protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Expressing, Infection, Quantitative RT-PCR, Western Blot

    UK5099 alleviates MRMP-induced mitochondrial damage (A) mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey’s post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: UK5099 alleviates MRMP-induced mitochondrial damage (A) mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey’s post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Infection, Quantitative RT-PCR, Expressing, Western Blot

    UK5099 alleviates MRMP-induced pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay. (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: UK5099 alleviates MRMP-induced pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay. (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Lactate Dehydrogenase Assay, TUNEL Assay, Expressing, Infection, Western Blot

    MG132-mediated PINK1 deficiency induces mitochondrial damage. (A) Mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E,F) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MG132-mediated PINK1 deficiency induces mitochondrial damage. (A) Mitochondrial morphology was imaged using TEM ( n = 3). Scale bar: 500 nm. (B) Quantification of the average individual mitochondrial area ( n = 3). (C,D) mRNA levels in MRMP-infected HCAECs were determined using qRT-PCR ( n = 3). (E,F) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Infection, Quantitative RT-PCR, Expressing, Western Blot

    MG132-mediated PINK1 deficiency induces pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay ( n = 3). (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MG132-mediated PINK1 deficiency induces pyroptosis of HCAECs. (A,B) Cytokine release was determined using ELISA ( n = 3). (C) Cell viability was determined using CCK-8 assay ( n = 3). (D) Cytotoxicity was determined using LDH assay ( n = 3). (E,F) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (G–J) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Lactate Dehydrogenase Assay, TUNEL Assay, Expressing, Infection, Western Blot

    MPC1 induces pyroptosis of HCAECs via inhibiting PINK1-dependent mitophagy. (A–D) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). (E,F) Cytokine release was determined using ELISA ( n = 3). (G) Cell viability was determined using CCK-8 assay ( n = 3). (H) Cytotoxicity was determined using LDH assay ( n = 3). (I,J) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (K–N) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Journal: Frontiers in Pediatrics

    Article Title: MPC1 promotes the damage of human coronary endothelial cells in macrolide-resistant mycoplasma pneumoniae via inhibiting mitophagy

    doi: 10.3389/fped.2026.1731155

    Figure Lengend Snippet: MPC1 induces pyroptosis of HCAECs via inhibiting PINK1-dependent mitophagy. (A–D) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). (E,F) Cytokine release was determined using ELISA ( n = 3). (G) Cell viability was determined using CCK-8 assay ( n = 3). (H) Cytotoxicity was determined using LDH assay ( n = 3). (I,J) Cell death was determined using TUNEL assay ( n = 3). Scale bar: 50 μm. (K–N) Protein expression in MRMP-infected HCAECs was determined using Western blot ( n = 3). ** p < 0.01, one-way ANOVA followed by Tukey's post hoc test.

    Article Snippet: Human coronary endothelial cells (HCAECs) were purchased from ATCC, USA.

    Techniques: Expressing, Infection, Western Blot, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Lactate Dehydrogenase Assay, TUNEL Assay