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human coronary artery endothelial cells  (PromoCell)


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    Structured Review

    PromoCell human coronary artery endothelial cells
    (a-c) SM22α, eNOS, αSMA, and Fibronectin (FN) mRNA levels determined by qRT-PCR in human coronary artery <t>endothelial</t> cells (HCAEC) following treatment with TGFβ1 (10 ng/ml, 7d), hypoxia (5% O 2 , 4d) or TGFβ1 plus hypoxia (4d), in the absence or presence of ethanol (EtOH) at concentrations indicated (0-100 mM range). (d) SM22α, eNOS, and Cdh5 mRNA levels in HCAEC treated with TGFβ1 (10 mg/ml, 2d) +/- EtOH 25 mM or 100 mM. (e) Representative western blots showing CD31, Cdh5, SM22α, and SNAIL protein expression in HCAEC treated with TGFβ1, IL-1β, or Hypoxia +/- EtOH (25 mM or 100 mM). β-actin or GAPDH were used as loading controls. Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.
    Human Coronary Artery Endothelial Cells, supplied by PromoCell, used in various techniques. Bioz Stars score: 96/100, based on 259 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human coronary artery endothelial cells/product/PromoCell
    Average 96 stars, based on 259 article reviews
    human coronary artery endothelial cells - by Bioz Stars, 2026-06
    96/100 stars

    Images

    1) Product Images from "A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition"

    Article Title: A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition

    Journal: bioRxiv

    doi: 10.64898/2026.04.14.718463

    (a-c) SM22α, eNOS, αSMA, and Fibronectin (FN) mRNA levels determined by qRT-PCR in human coronary artery endothelial cells (HCAEC) following treatment with TGFβ1 (10 ng/ml, 7d), hypoxia (5% O 2 , 4d) or TGFβ1 plus hypoxia (4d), in the absence or presence of ethanol (EtOH) at concentrations indicated (0-100 mM range). (d) SM22α, eNOS, and Cdh5 mRNA levels in HCAEC treated with TGFβ1 (10 mg/ml, 2d) +/- EtOH 25 mM or 100 mM. (e) Representative western blots showing CD31, Cdh5, SM22α, and SNAIL protein expression in HCAEC treated with TGFβ1, IL-1β, or Hypoxia +/- EtOH (25 mM or 100 mM). β-actin or GAPDH were used as loading controls. Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.
    Figure Legend Snippet: (a-c) SM22α, eNOS, αSMA, and Fibronectin (FN) mRNA levels determined by qRT-PCR in human coronary artery endothelial cells (HCAEC) following treatment with TGFβ1 (10 ng/ml, 7d), hypoxia (5% O 2 , 4d) or TGFβ1 plus hypoxia (4d), in the absence or presence of ethanol (EtOH) at concentrations indicated (0-100 mM range). (d) SM22α, eNOS, and Cdh5 mRNA levels in HCAEC treated with TGFβ1 (10 mg/ml, 2d) +/- EtOH 25 mM or 100 mM. (e) Representative western blots showing CD31, Cdh5, SM22α, and SNAIL protein expression in HCAEC treated with TGFβ1, IL-1β, or Hypoxia +/- EtOH (25 mM or 100 mM). β-actin or GAPDH were used as loading controls. Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.

    Techniques Used: Quantitative RT-PCR, Western Blot, Expressing, Control

    (a) (b) Representative images of immunofluorescently stained carotid cross sections from sham-operated and ligated controls, moderate EtOH, and Binge EtOH experimental groups (males). Blue = Dapi nuclear stain, red = Tm-Cdh5+, and white=αSMA+. (c) Cells co-expressing Cdh5 and αSMA (i.e., myo-endothelial cells indicative of EndMT) were quantified using QuPath bioimage analysis software in carotid cross sections post-ligation from controls (grey bars), moderate EtOH (green bars), and binge EtOH (red bars) experimental groups. Bar graphs show cumulative data expressed as % Myoendothelial cells /full cross section, % Myoendothelial cells /neointima, or Number of myoendothelial cells/full cross section. Data are mean±SEM, n=25-30 sections from 5-6 mice). *p<0.05, ** P<0.001, **** p<0.0001.
    Figure Legend Snippet: (a) (b) Representative images of immunofluorescently stained carotid cross sections from sham-operated and ligated controls, moderate EtOH, and Binge EtOH experimental groups (males). Blue = Dapi nuclear stain, red = Tm-Cdh5+, and white=αSMA+. (c) Cells co-expressing Cdh5 and αSMA (i.e., myo-endothelial cells indicative of EndMT) were quantified using QuPath bioimage analysis software in carotid cross sections post-ligation from controls (grey bars), moderate EtOH (green bars), and binge EtOH (red bars) experimental groups. Bar graphs show cumulative data expressed as % Myoendothelial cells /full cross section, % Myoendothelial cells /neointima, or Number of myoendothelial cells/full cross section. Data are mean±SEM, n=25-30 sections from 5-6 mice). *p<0.05, ** P<0.001, **** p<0.0001.

    Techniques Used: Staining, Expressing, Software, Ligation



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    (a-c) SM22α, eNOS, αSMA, and Fibronectin (FN) mRNA levels determined by qRT-PCR in human coronary artery <t>endothelial</t> cells (HCAEC) following treatment with TGFβ1 (10 ng/ml, 7d), hypoxia (5% O 2 , 4d) or TGFβ1 plus hypoxia (4d), in the absence or presence of ethanol (EtOH) at concentrations indicated (0-100 mM range). (d) SM22α, eNOS, and Cdh5 mRNA levels in HCAEC treated with TGFβ1 (10 mg/ml, 2d) +/- EtOH 25 mM or 100 mM. (e) Representative western blots showing CD31, Cdh5, SM22α, and SNAIL protein expression in HCAEC treated with TGFβ1, IL-1β, or Hypoxia +/- EtOH (25 mM or 100 mM). β-actin or GAPDH were used as loading controls. Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.
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    Image Search Results


    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

    (a-c) SM22α, eNOS, αSMA, and Fibronectin (FN) mRNA levels determined by qRT-PCR in human coronary artery endothelial cells (HCAEC) following treatment with TGFβ1 (10 ng/ml, 7d), hypoxia (5% O 2 , 4d) or TGFβ1 plus hypoxia (4d), in the absence or presence of ethanol (EtOH) at concentrations indicated (0-100 mM range). (d) SM22α, eNOS, and Cdh5 mRNA levels in HCAEC treated with TGFβ1 (10 mg/ml, 2d) +/- EtOH 25 mM or 100 mM. (e) Representative western blots showing CD31, Cdh5, SM22α, and SNAIL protein expression in HCAEC treated with TGFβ1, IL-1β, or Hypoxia +/- EtOH (25 mM or 100 mM). β-actin or GAPDH were used as loading controls. Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.

    Journal: bioRxiv

    Article Title: A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition

    doi: 10.64898/2026.04.14.718463

    Figure Lengend Snippet: (a-c) SM22α, eNOS, αSMA, and Fibronectin (FN) mRNA levels determined by qRT-PCR in human coronary artery endothelial cells (HCAEC) following treatment with TGFβ1 (10 ng/ml, 7d), hypoxia (5% O 2 , 4d) or TGFβ1 plus hypoxia (4d), in the absence or presence of ethanol (EtOH) at concentrations indicated (0-100 mM range). (d) SM22α, eNOS, and Cdh5 mRNA levels in HCAEC treated with TGFβ1 (10 mg/ml, 2d) +/- EtOH 25 mM or 100 mM. (e) Representative western blots showing CD31, Cdh5, SM22α, and SNAIL protein expression in HCAEC treated with TGFβ1, IL-1β, or Hypoxia +/- EtOH (25 mM or 100 mM). β-actin or GAPDH were used as loading controls. Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.

    Article Snippet: Human coronary artery endothelial cells (HCAEC, C-12221) and Human umbilical vein endothelial cells (HUVEC-pooled, C-12203) were obtained from PromoCell.

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

    (a) (b) Representative images of immunofluorescently stained carotid cross sections from sham-operated and ligated controls, moderate EtOH, and Binge EtOH experimental groups (males). Blue = Dapi nuclear stain, red = Tm-Cdh5+, and white=αSMA+. (c) Cells co-expressing Cdh5 and αSMA (i.e., myo-endothelial cells indicative of EndMT) were quantified using QuPath bioimage analysis software in carotid cross sections post-ligation from controls (grey bars), moderate EtOH (green bars), and binge EtOH (red bars) experimental groups. Bar graphs show cumulative data expressed as % Myoendothelial cells /full cross section, % Myoendothelial cells /neointima, or Number of myoendothelial cells/full cross section. Data are mean±SEM, n=25-30 sections from 5-6 mice). *p<0.05, ** P<0.001, **** p<0.0001.

    Journal: bioRxiv

    Article Title: A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition

    doi: 10.64898/2026.04.14.718463

    Figure Lengend Snippet: (a) (b) Representative images of immunofluorescently stained carotid cross sections from sham-operated and ligated controls, moderate EtOH, and Binge EtOH experimental groups (males). Blue = Dapi nuclear stain, red = Tm-Cdh5+, and white=αSMA+. (c) Cells co-expressing Cdh5 and αSMA (i.e., myo-endothelial cells indicative of EndMT) were quantified using QuPath bioimage analysis software in carotid cross sections post-ligation from controls (grey bars), moderate EtOH (green bars), and binge EtOH (red bars) experimental groups. Bar graphs show cumulative data expressed as % Myoendothelial cells /full cross section, % Myoendothelial cells /neointima, or Number of myoendothelial cells/full cross section. Data are mean±SEM, n=25-30 sections from 5-6 mice). *p<0.05, ** P<0.001, **** p<0.0001.

    Article Snippet: Human coronary artery endothelial cells (HCAEC, C-12221) and Human umbilical vein endothelial cells (HUVEC-pooled, C-12203) were obtained from PromoCell.

    Techniques: Staining, Expressing, Software, Ligation