primary human umbilical vein endothelial cells huvec  (PromoCell)

Journal: iScience

Article Title: Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis

doi: 10.1016/j.isci.2026.115028

Figure Lengend Snippet: Regulatory role of HSPB1 in endothelial cell EndoMT (A) Western blot shows HSPB1 expression in HUVECs following lentiviral-mediated overexpression (LV-HSPB1) or knockdown (LV-HSPB1-RNAi); β-actin served as a loading control. (B) Quantification of HSPB1/β-actin ratio shows significant differences between groups. (C) Representative images of Transwell migration assays evaluating the effect of HSPB1 on TGF-β1–induced endothelial migration (scale bars, 100 μm). (D) Quantification of migrated cells per field. (E) Representative tube formation images showing the effect of HSPB1 modulation on TGF-β1–induced angiogenic activity (scale bars, 200 μm). (F–H) Quantitative analysis of tube formation parameters, including the number of branches (F), loops (G), and total tube length (H), measured using ImageJ software. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.

Article Snippet: Human umbilical vein endothelial cells (HUVECs) , ATCC , Primary cells, pooled donors.

Techniques: Western Blot, Expressing, Over Expression, Knockdown, Control, Migration, Activity Assay, Software

Journal: iScience

Article Title: Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis

doi: 10.1016/j.isci.2026.115028

Figure Lengend Snippet: Effects of HSPB1 on signaling pathways and TGF-β secretion in HUVECs under hypoxic conditions (A and B) HUVECs were transfected with adenoviral vectors for HSPB1 overexpression (OE) or knockdown (KD) and cultured for 48 h before RNA extraction. Gene expression analysis was performed using RNA sequencing. Gene set enrichment analysis (GSEA) assessed the regulatory roles of HSPB1 in processes such as heart development, angiogenesis, and cell proliferation (A). Further analysis using Hallmark gene sets explored HSPB1 signaling pathway activation (B). (C–G) Following transfection, HUVECs were cultured for 24 h and subjected to hypoxic conditions (3% O 2 ) for 48 h. Western blot analysis of the indicated proteins was performed. (D) pSmad2/3/Smad2/3 ratio, (E) quantification of CD31 protein expression, (F) quantification of E-cadherin expression, (G) quantification of α-SMA expression, and (H) quantification of N-cadherin expression were measured relative to β-actin. (I) TGF-β levels were measured by ELISA in cell supernatants. Data are presented as mean ± SD ( n ≥ 6). Exact p values are indicated in the graphs. Statistical analyses were performed using one-way ANOVA followed by a Bonferroni post hoc test.

Article Snippet: Human umbilical vein endothelial cells (HUVECs) , ATCC , Primary cells, pooled donors.

Techniques: Protein-Protein interactions, Transfection, Over Expression, Knockdown, Cell Culture, RNA Extraction, Gene Expression, RNA Sequencing, Activation Assay, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: (A) Effects of different concentrations of rosuvastatin (0.1, 1, 5 and 10 µM) on HUVEC viability for 24 h. (B) Effects of treatment with different concentrations of ox-LDL (50, 100 and 200 µg/mL) for 24 h on HUVEC viability. (C) HUVECs were treated with different concentrations of rosuvastatin and ox-LDL (200 µg/ml) for 24 h. * P < 0.05, *** P < 0.001 by one-way ANOVA. (D) Bar chart showing the signaling pathways enriched with DEGs in the RNA-Seq dataset ( GSE206927 ) of ox-LDL-treated HUVECs according to GO analysis. (E) Bubble chart showing the signaling pathways enriched with DEGs according to KEGG analysis. (F-G) HUVECs stimulated with ox-LDL and different concentrations of rosuvastatin were stained with DAPI (blue) and Ki67 (purple). Ki67-positive cells were quantified, bar = 100 μm, * P < 0.05, **** P < 0.0001 by one-way ANOVA.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Protein-Protein interactions, RNA Sequencing, Staining

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: HUVECs were treated with ox-LDL in the presence or absence of different concentrations of rosuvastatin (0.1, 1, 5 and 10 µM) for 24 h. (A) NO production in HUVECs. (B) eNOS mRNA expression in HUVECs. (C) A microplate reader was used to measure the fluorescence intensity of the ROS at an excitation wavelength of 488 nm and an absorption wavelength of 525 nm via a fluorescent probe DCFH-DA kit, and Rosup was used as a positive control. (D) The mean intracellular fluorescence intensity was analyzed via fluorescence microscopy. The data are presented as the mean ± SEM. * P < 0.05, ** P < 0.01, ** P < 0.0001 by one-way ANOVA.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Expressing, Fluorescence, Positive Control, Microscopy

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: (A-B) Bcl2 and Bax mRNA expression in HUVECs treated with different concentrations of rosuvastatin and ox-LDL (200 µg/ml) for 24 h. ** P < 0.01, *** P < 0.001, **** P < 0.0001 by one-way ANOVA. (C-D) BCL-2 and Bax protein expression in HUVECs treated with different concentrations of rosuvastatin and ox-LDL (200 µg/ml) for 24 h. The data are presented as the means ± SEMs. * P < 0.05 by one-way ANOVA. (E) HUVECs stimulated with ox-LDL and different concentrations of rosuvastatin were stained with DAPI (blue), Bax (green) and mitochondria (red); scale bar = 20 μm. (F) Early and late apoptosis of HUVECs treated with 100 µg/mL ox-LDL and 10 μmol/L rosuvastatin for 24 h. The quantification results are shown on the right (n = 5). *** P < 0.001, **** P < 0.0001 by one-way ANOVA.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Expressing, Staining

Journal: PLOS One

Article Title: Rosuvastatin protects against oxLDL-induced endothelial cell oxidative stress and attenuates atherosclerotic plaque formation in ApoE -/- mice through the NF-κB pathway

doi: 10.1371/journal.pone.0339967

Figure Lengend Snippet: (A-D) Protein levels of IkBα, p-IkBα, P65 and p-P65 in HUVECs treated with or without 10 µM rosuvastatin and treated with 100 µg/mL ox-LDL for 24 h. The data are presented as the means ± SEMs. * P < 0.05, ** P < 0.01 by one-way ANOVA. (E) Schematic diagram illustrating the role of rosuvastatin in ox-LDL-induced endothelial cell dysfunction. Rosuvastatin regulates oxidative stress and apoptosis-related gene transcription in endothelial cells by inhibiting ox-LDL-induced IKBα and P65 activation in endothelial cells.

Article Snippet: Primary human umbilical vein endothelial cells (HUVECs) (Cat#PCS-100–010, ATCC, Maryland, USA) were maintained in vascular cell basal medium (Cat#PCS-100–030, ATCC, Maryland, USA) containing ascorbic acid (Cat#PCS-999–006, ATCC, Maryland, USA), FBS (Cat#PCS-999–010, ATCC, Maryland, USA), rhEGF (Cat#PCS-999–018, ATCC, Maryland, USA), heparin sulfate (Cat#PCS-999–011, ATCC, Maryland, USA), L-glutamine (Cat#PCS-999–017, ATCC, Maryland, USA), rhVEGF (Cat#PCS-999–024, ATCC, Maryland, USA), rhFGF-b (Cat#PCS-999–020, ATCC, Maryland, USA), rhIGF-1 (Cat#PCS-999–021, ATCC, Maryland, USA), and hydrocortisone (Cat#PCS-999–014, ATCC, Maryland, USA) at 37°C in an atmosphere containing 5% CO 2 .

Techniques: Activation Assay