dermal microvascular endothelial cells hdmec  (PromoCell)

Journal: bioRxiv

Article Title: IFITM1 inhibits Henipavirus membrane fusion by trapping ephrinB2 receptors in fusion-unfavorable membrane nanodomains

doi: 10.64898/2026.05.06.723334

Figure Lengend Snippet: The role of endogenous IFITMs in NiV and HeV pseudovirus entry into human endothelial and epithelial cells. The endogenous IFITMs mRNA levels in HuMEC ( a-c ) and HEK293T cells ( g-i ). Cells were transfected with siRNAs targeting IFITM proteins and scrambled siRNA (NC). IFN-α2b was used to stimulate the expression of IFITM proteins. The mRNA expression levels were detected using qPCR and normalized to that of NC at the untreated condition (-IFN-α). d and j , endogenous IFITM1,2,3 proteins expression in HuMEC ( d ) and HEK293T cells ( j ) upon siRNA knockdown analyzed by Western Blot. IFITMs were detected by anti-IFITM antibodies, and GAPDH was a loading control. The entry of NiV/VSV pp and HeV/VSV pp to HuMEC ( e and f ) and HEK293T cells ( k and l ). NiV and HeV glycoproteins were pseudotyped to VSV particles in which the VSV-G gene was replaced with the Renilla luciferase gene. Virus entry was measured by luminescence intensity and normalized to that of scrambled siRNA at the untreated condition (NC, −IFN-α). Virus entry levels in siRNA-transfected cells were compared with those transfected with scrambled siRNA (NC) under respective −IFN-α and +IFN-α conditions. Virus entry in IFN-α–treated cells (+IFN-α) was further compared with that in resting cells (−IFN-α) and labeled with a bracket. Bars represent means ± SEM. Results from at least 3 independent experiments are shown. p values were obtained using one-way analysis of variance (ANOVA) with post hoc correction (nonsignificant [ns], p > 0.05; *, p ≤ 0.05; **, p ≤ 0.01; ***, p ≤ 0.001; ****, p ≤ 0.0001).

Article Snippet: Human microvascular endothelial cells (HuMEC) (ATCC CRL-4060) were cultured in Vascular cell basal medium (ATCC, PCS-100-030) with Microvascular endothelial cell growth kit – BBE (ATCC, PCS-110-040) and 0.5 ug/ml puromycin (10 mg/ml stock, Gibco A1138-03).

Techniques: Transfection, Expressing, Knockdown, Western Blot, Control, Luciferase, Virus, Labeling

Journal: iScience

Article Title: DPPA inhibits melanoma by targeting angiogenesis through activating autocrine IFN-γ-CXCL9/10/11-CXCR3 axis in vascular endothelial cells

doi: 10.1016/j.isci.2026.116309

Figure Lengend Snippet: DPPA suppresses angiogenesis through the activation of the IFN-γ-CXCL9/10/11-CXCR3 axis in vascular endothelial cells (A) Angiogenesis PCR array for human dermal microvascular endothelial cells (HDMECs) treated with DMSO and DPPA at a concentration of 10 μM for 48 h. The relative expression levels were calculated as the log2 fold change, and the differentially expressed genes were selected on the basis of a log2 ≤ −2 or ≥2. (B) KEGG classification of differentially expressed genes in A. HDMECs were treated with DMSO and DPPA (10 μM) for 48 h, and RNAs and proteins were collected to analyze the expression of the IFN-γ-CXCL9/10/11 axis at both the transcriptional and protein levels using RT-qPCR (C) and western blotting (D) assays. n = 3 technical replicates from 3 biological replicates for each group. (E) 3D models of docking poses for DPPA and receptors (including IFN-γ, CXCL9, CXCL10, and CXCL11) predicted by Autodock Vina Tools. (F) 2D model of the interaction between DPPA and IFN-γ. HDMECs were treated with IFN-γ for 48 h, after which the RNAs and proteins were collected and subjected to RT-qPCR (G) and western blotting (H) to quantify the expression levels of CXCL9, CXCL10, CXCL11, p65, and pp65. β-actin was served as an internal control. (G) n = 3 technical replicates from 3 biological replicates for each group. (H) n = 3 biological replicates for each group. (I) HDMECs were treated with NF-κB inhibitor (NF-κB-IN-11) for 48 h, and RNAs were collected to analyze the expression of the IFN-γ at the transcriptional levels using qRT-PCR. β-actin was served as an internal control. n = 3 biological replicates for each group. Cell migration (J) and tube formation on Matrigel (K) of HDMECs treated with DMSO, DPPA, or DPPA with CXCL9/10/11-CXCR3 axis-blocking neutralizing antibodies. n = 3 technical replicates from 3 biological replicates for each group. Scale bars: 100 μm. Data are presented as mean ± SD. Significant effects: p values were calculated using Student’s t test (two-tailed unpaired t test) for C, D, G, H, and I, and one-way ANOVA for J and K. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001 and ns: p > 0.05 (compared with the control/DMSO group).

Article Snippet: Human dermal microvascular endothelial cells (HDMECs, Procell system, Wuhan, China) were maintained in endothelial cell growth medium supplemented with growth supplements (EGM, CC-3124, Lonza), and have been authenticated by Procell system using CD31 immunofluorescence (IF) staining and been tested for mycoplasma contamination.

Techniques: Activation Assay, Concentration Assay, Expressing, Quantitative RT-PCR, Western Blot, Control, Migration, Blocking Assay, Two Tailed Test

Journal: medRxiv

Article Title: Feasibility of Endothelial Cell Isolation from Routine Coronary Function Testing in ANOCA Patients

doi: 10.64898/2026.04.09.26350551

Figure Lengend Snippet: A) Method to isolate and culture ECs from catheterization material used during coronary function testing. B) Representative morphology (I, passage 0) and immunofluorescence images of cultured ECs (II and III, passage 5) showing positivity for VE-cadherin (II), von Willebrand Factor (vWF) (II) and CD31 (III). C) Flow-cytometric characterization of cultured ECs (passage 1) in comparison with multiple reference cell populations, including human dermal microvascular ECs (HDMVEC), human cardiac microvascular ECs (HCMEC), human coronary artery ECs (HCAEC), human plaque myofibroblasts and mesenchymal stem cells (MSC). The plotted histograms depict the ‘relative counts’ on the y-axis and the ‘relative intensity’ on the x-axis

Article Snippet: Reference populations included human dermal microvascular ECs (HDMVEC; iXCells Biotechnologies, REF#10HU-019), human cardiac microvascular ECs (HCMEC; Sigma-Aldrich, REF#C-12285), human coronary artery ECs (HCAEC; Lonza, REF#CC-2585), human plaque myofibroblasts and mesenchymal stem cells (MSC; Cell Therapy Facility, University Medical Center Utrecht; code: MSC053P3_AL-MSC071P3_R).

Techniques: Immunofluorescence, Cell Culture, Comparison