human coronary artery endothelial cells  (PromoCell)

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

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

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

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

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

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

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

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

Journal: Journal of Extracellular Vesicles

Article Title: The Fatty Acid Transporter CD36 Mediates Uptake, Biodistribution, and Cardioprotection by Small Extracellular Vesicles From HEK293 Cells

doi: 10.1002/jev2.70254

Figure Lengend Snippet: Dose‐response and time‐response uptake of HEK293‐sEVs in human endothelial cells and cardiomyocytes. (A–C) Human coronary artery and coronary microvascular endothelial cells (HCAEC and HCMEC respectively) and human umbilical vein endothelial cells (HUVEC) were treated for 4 h with increasing doses of HEK293‐sEVs. A linear dose‐response was revealed in all endothelial cells, as a 10‐fold increase of sEVs dose results in a 10‐fold increase of cellular uptake (Nluc Nanoluciferase activity). (D–F) sEVs rapidly internalise endothelial cells ((D) HCAEC, (E) HCMEC, and (F) HUVEC) within the first hour of incubation reaching the highest intracellular localisation after 4 h, corresponding to higher Nluc activity. A reduction in luciferase activity after 24 h is observed in all endothelial cells, reflective of the reduced amount of sEVs intracellularly. (G) Uptake of HEK293‐sEVs in adult rat cardiomyocytes is slow and time‐dependent, and high Nluc activity is recorded only after 24 h of sEVs incubation. Data shown as mean ± SEM ( n = 4). * p < 0.05, ** p < 0.01, **** p < 0.0001.

Article Snippet: HCMEC (human coronary microvascular endothelial cells) and HCAEC (human coronary artery endothelial cells) were cultured in endothelial cell basal medium MV‐2 (PromoCell, C‐22022) supplemented with the supplement mix (PromoCell, C‐39226).

Techniques: Activity Assay, Incubation, Luciferase