promocell microvascular media  (PromoCell)

Journal: bioRxiv

Article Title: Human iPSC-derived CNS and retinal microvasculature-on-a-chip models recapitulate hallmarks of diabetic microvascular pathology

doi: 10.64898/2026.01.15.699708

Figure Lengend Snippet: Gene expression changes in CNS-mv-on-a-chip induced by high glucose level. (A) The principal component analysis (PCA) plot shows clustering of samples cultured under physiological (5.5 mM glucose) and hyperglycemic (75 mM glucose) conditions. (B) Volcano plot illustrating differentially expressed genes between physiological and hyperglycemic CNS-mv-on-a-chip conditions. Orange and blue dots represent significantly upregulated and downregulated genes, respectively (FDR < 0.05, |FC| >2). (C) Heatmap showing upregulated genes associated with inflammation. Values are shown as fold changes relative to control group mean. (D) Over-representation analysis (ORA) plot of genes upregulated under hyperglycemia conditions. (E) Quantitative PCR analysis of IL1B, JUN and NFKBIA expression in ECs and PCs isolated from CNS-mv-on-a-chip cultured under physiological 5.5 mM glucose concentration (5.5G), hyperglycemic conditions 25 mM (25G) and 75 mM glucose (75G), or corresponding osmotic controls with mannitol (19.5M and 69.5M). Gene expression was normalized to GAPDH and HMBS as housekeeping genes and calculated using the ΔΔCt method. Data are presented as mean ± SD, n = 3-4.

Article Snippet: CD31 + ECs were cultured on 0.2 % gelatin-coated plates in MV medium (PromoCell, C-22020) that contains physiological (5.5 mM) glucose level supplemented with 30 ng/ml VEGF-A and 20 ng/ml FGF-2.

Techniques: Gene Expression, Cell Culture, Control, Real-time Polymerase Chain Reaction, Expressing, Isolation, Concentration Assay

Journal: Nature Communications

Article Title: Pericytes orchestrate a tumor-restraining microenvironment in glioblastoma

doi: 10.1038/s41467-025-66985-1

Figure Lengend Snippet: A UMAP plot of 16,086 Pdgfb ret/ret and 42,838 Pdgfb ret /+ cells that were isolated from a total of 4 and 7 tumors, respectively, and analyzed with scRNA-seq. The UMAP clusters are colored based on cell identity as cycling tumor cells I-IV (CT I-IV), mixed OPC-like/NPC-like tumor cells I-II (mOPC/NPC I-II), mixed mesenchymal/OPC-like/NPC-like/IFN tumor cells (mMES/OPC/NPC/IFN), astrocytes/AC-like tumor cells (AC), mesenchymal tumor cells I-II (MES I-II), tumor oligodendrocytes (tOLIG), oligodendrocytes (OLIG), activated microglia (AM), microglia (MG), macrophages (MP), NK/T/NKT cells (NKT), dendritic cells (DC), perivascular cells/pericytes (PC), endothelial cells (EC), ependymal cells (EP) and platelets (PL). B Clustered dot plot showing the scaled average expression of selected top differentially expressed genes across all clusters. C Feature plot showing the log-normalized expression of the RCAS-unique vector sequence across all clusters. D Clustered correlation matrix showing pairwise Pearson’s correlation coefficients of the mean Z -score per cell estimated for different cell identity signatures from this study, Neftel et al. (nef), and Couturier et al. (cou). Black boxes highlight selected clustered signatures. E Butterfly plot of molecular subtype signature scores defined by Neftel et al. The quadrants correspond to the four subtypes: mesenchymal-like (MES-like), neural-progenitor-like (NPC-like), astrocyte-like (AC-like), and oligodendrocyte-progenitor-like (OPC-like). The position of each cell reflects its relative signature score across both axes. Colors represent the different clusters, as in ( A ). Source data are provided as a file.

Article Snippet: Endothelial cells were cultured in endothelial cell medium (PromoCell, C-22020).

Techniques: Isolation, Expressing, Plasmid Preparation, Sequencing

Journal: Nature Communications

Article Title: Pericytes orchestrate a tumor-restraining microenvironment in glioblastoma

doi: 10.1038/s41467-025-66985-1

Figure Lengend Snippet: A Immunostainings of PODXL in Pdgfb ret/ret and Pdgfb ret/+ p53 −/− / H-Ras tumor cell-induced glioma sections. B Assessment of glioma tissue parameters, comparing Pdgfb ret/ret ( n = 7) and Pdgfb ret/+ ( n = 7) tissue sections of p53 −/− / H-Ras gliomas based on PODXL expression. Each dot represents the average of several FOVs in one tumor, taken at different positions. Area p = 0.0091, t = 3.064, df = 13. Length, p = 0.0025, t = 3.738, df = 13. Juntion p = 0.0006, t = 4.511, df = 13. C Fluorescence images (left) and quantification (right) of a vessel functionality dextran (70 kDa) analysis comparing p53 −/− / H-Ras Pdgfb ret/ret and Pdgfb ret/+ tumors. Dextran-positive areas were quantified and related to the PECAM1 + area. Each dot represents a tumor section, p = 0.0212, t = 2.370, df = 14. D , E Quantification of tumor cell infiltration at the invasive rim (IR) in PDGFB-induced Pdgfb ret/ret and Pdgfb ret/+ tumors, based on PECAM1 and OLIG2 stainings. IR was defined as the FOV portion adjacent to the tumor core (white dotted line) ( D ). Vessel co-opting tumor cells were defined as OLIG2 + cells in contact with PECAM + cells and normalized to total OLIG2 + cells. Each dot represents a FOV. Pdgfb ret/ret ( n = 17) and Pdgfb ret/+ ( n = 22), p = 0.0038, t = 3.085, df = 37 ( E ). F PECAM1 + cell-associated CD206 + macrophages ( Pdgfb ret/ret ). Arrows indicate CD206 + cells adjacent to PECAM1 + cells. G Quantification of CD206 + /CD11B + /F4/80 + macrophages (left) and CD11B + /LY6C + /LY6G − myeloid-derived suppressor cells (MDSC, right), comparing PDGFB-induced Pdgfb ret/ret ( n = 10) and Pdgfb ret/+ ( n = 8) tumors. Left panel p = 0.0212, t = 2.555, df = 16. Right panel p = 0.0447, t = 2.178, df = 16. H Scaled average expression of macrophage polarization markers in the scRNA-seq dataset, comparing Pdgfb ret/ret and Pdgfb ret/+ cells. I Chord diagrams of pathways that exhibit different signaling patterns between Pdgfb ret/ret and Pdgfb ret/+ tumors. TEdge weights are proportional to the estimated interaction strength. Left and middle panel: CSF pathway (active in both Pdgfb ret/ret and Pdgfb ret/+ tumors); right panel: CD200 pathway (active exclusively in Pdgfb ret/ret tumors). J Quantification of CD206 + macrophages, cultured with pericyte- or endothelial cell-primed or mock medium. Either IL4, IFNγ, or no cytokine was added to the cultures. Analysis was performed 48 h post addition of primed media. Median with 95% CI is shown. Pdgfb ret/+ cell co-cultures are depicted in black ( n = 3) and Pdgfb ret/ret in red ( n = 3). Two-sided t -test. Median is indicated ( B , C , E , G , J ). * p < 0.05, ** p < 0.01, *** p < 0.001, ns not significant. Source data are provided as a file.

Article Snippet: Endothelial cells were cultured in endothelial cell medium (PromoCell, C-22020).

Techniques: Expressing, Fluorescence, Derivative Assay, Cell Culture

Journal: PLOS Neglected Tropical Diseases

Article Title: Differential restriction of chikungunya virus in primary human cardiac endothelial cells occurs at multiple steps in the viral life cycle

doi: 10.1371/journal.pntd.0012534

Figure Lengend Snippet: Human primary ( A ) cardiac fibroblasts, ( B ) aortic smooth muscle cells, ( C ) cardiac myocytes, and ( D ) cardiac microvascular endothelial cells were infected with MAYV, ZIKV, RVFV MP-12, or LACV at a MOI of 0.1. Supernatant was collected at 0, 6, 24, 48, and 72 hpi, and viral titers were quantified by plaque assay. Data points represent the mean of two independent experiments (n=4), with error bars representing the SEM. The limit of detection is indicated by the gray shaded area.

Article Snippet: Primary human cardiac microvascular endothelial cells from Donor #1 (hCMEC, PromoCell, C-12285) were grown in Endothelial Cell Growth Media MV (PromoCell, C-22020) and cells from Donor #2 (HMVEC-C, Lonza, CC-7030), a gift from Dr. Tessa Barrett at the NYU Grossman School of Medicine were grown in EGM-2 MV Microvascular Endothelial Cell Growth Medium-2 BulletKit (Lonza, CC-3202).

Techniques: Infection, Plaque Assay

Journal: PLOS Neglected Tropical Diseases

Article Title: Differential restriction of chikungunya virus in primary human cardiac endothelial cells occurs at multiple steps in the viral life cycle

doi: 10.1371/journal.pntd.0012534

Figure Lengend Snippet: ( A , B) HCMECs were pre-treated with 5 µM ruxolitinib or mock-treated for 2 days, then infected with CHIKV IOL ZsGreen at a MOI of 0.1 for 1 hour. Post-infection, cells were incubated with media supplemented with or without 5 µM ruxolitinib and fixed for high-content microscopy at 5 dpi. (A) Quantification of percent infected cells as measured by CHIKV-IOL-ZsGreen positive cells relative to number of total cells measured by DAPI staining. (B) Representative images from a CX7 high-content microscope showing cell nuclei stained with DAPI (blue channel) and CHIKV-IOL-ZsGreen infected cells (green channel). (C) Dot plot showing normalized expression levels of IFITM1, IFITM2, IFITM3, BST2, and CD74 in cardiac smooth muscle cells (CSMC), cardiac fibroblasts (CF), cardiac myocytes (CM), cardiac microvascular endothelial cells (CMEC), and pulmonary endothelial cells (PMEC) using the Tabula Sapiens dataset. ( D and E) Representative images of western blots visualizing actin, IFITM2, and IFITM3 protein levels. (D) HCMECs were treated with 5 µM ruxolitinib for 2, 4, or 6 days or mock-treated. Cells were collected in laemmli buffer, proteins were separated by SDS-PAGE and visualized by immunoblotting. ( E , F) HCMECs, hBMECs, hPMECs, and hCFs were treated with IFNβ or mock-treated for 24 hours. Cells were harvested and proteins analyzed as described above. (E) Values indicate relative intensity of expression as compared to hCMEC basal expression, with SD. (F) Quantified IFITM2 and IFITM3 expression after 24 hours IFNβ treatment. Data represents the mean of n = 3 independent trials in technical triplicate ( A, B ) with error bars showing the SEM and the limit of detection indicated by the gray shaded area. Western blots represent at least n = 2 independent trials ( D-F ). Statistical significance ( A ) was found by a Kruskal-Wallis test with multiple comparisons, with p-values representing *p<0.05.

Article Snippet: Primary human cardiac microvascular endothelial cells from Donor #1 (hCMEC, PromoCell, C-12285) were grown in Endothelial Cell Growth Media MV (PromoCell, C-22020) and cells from Donor #2 (HMVEC-C, Lonza, CC-7030), a gift from Dr. Tessa Barrett at the NYU Grossman School of Medicine were grown in EGM-2 MV Microvascular Endothelial Cell Growth Medium-2 BulletKit (Lonza, CC-3202).

Techniques: Infection, Incubation, Microscopy, Staining, Expressing, Western Blot, SDS Page