Journal: bioRxiv

Article Title: Using atorvastatin-induced vascular weakness to model brain haemorrhage in vascularised cerebral organoids

doi: 10.64898/2026.04.20.719465

Figure Lengend Snippet: ( A ) Phase contrast images of HBMECs after 24 hours of treatment with 100 μM atorvastatin (ATV). Scale bars 50 μm. ( B ) Cell survival after ATV treatment for 24 hours in both stationary and rotating culture conditions ( n =4 independent repeats). Scale bars 100 μm. ( C ) qPCR analysis of marker expression after ATV treatment in rotating cells shows an increase in VE-Cadherin and NG2 gene expression (non-significant, One-Way ANOVA). ( D ) Fluorescent images of CD31 (green) and ZO-1 (red) cellular expression after 24 hours with ATV and DMSO control. ( E ) Total expression of ZO-1 after treatment ( n =4 independent repeats, two-way ANOVA *** P =0.0009, **** P <0.0001) ( F ) Analysis of ZO-1 co-localised with CD31 on the cell surface when treated with ATV ( n =4 independent repeats, two-way ANOVA, *** P =0.0002). ( G ) Fluorescent images of CD31 (green) and VE-Cadherin (red) cellular expression after 24 hours of ATV treatment in both stationary (top panels) and rotating culture (bottom panels). Zoom inset shows the internalisation of both CD31 and VE-Cadherin from the cell surface when treated with ATV. Scale bars 20 μm. ( H ) Analysis of VE-Cadherin co-localised with CD31 on the cell surface when treated with ATV ( n =3 independent repeats, two-way ANOVA, * P <0.04). ( I ) Total area expression of CD31 and VE-Cadherin as a percentage area of DAPI in both stationary and rotating cells, ( n =3 independent repeats, no significance from analysis with a two-way ANOVA).

Article Snippet: Primary human brain microvascular endothelial cells (HBMECs) (Innoprot P10361) were maintained on 1% gelatin coated flasks in endothelial cell growth medium MV (PromoCell C-22020).

Techniques: Marker, Expressing, Gene Expression, Control

Journal: bioRxiv

Article Title: Using atorvastatin-induced vascular weakness to model brain haemorrhage in vascularised cerebral organoids

doi: 10.64898/2026.04.20.719465

Figure Lengend Snippet: ( A ) Representative images of filipin-stained HBMECs, after 24hours of drug treatment. Scale bars 50 μm. ( B ) Filipin expression as a percentage of area from 6 ROIs in 2 wells across 2 independent repeats after 24 hours with ATV, ** P =0.0081, t -test. ( C ) qPCR analysis of rotated HBMECs after 24 hours of drug treatment shows a significant increase in HMGCR expression ( n =5 independent repeats, * P =0.0323 One-Way ANOVA).

Article Snippet: Primary human brain microvascular endothelial cells (HBMECs) (Innoprot P10361) were maintained on 1% gelatin coated flasks in endothelial cell growth medium MV (PromoCell C-22020).

Techniques: Staining, Expressing

Journal: bioRxiv

Article Title: Using atorvastatin-induced vascular weakness to model brain haemorrhage in vascularised cerebral organoids

doi: 10.64898/2026.04.20.719465

Figure Lengend Snippet: ( A ) Phase images of tube formation in untreated and ATV-treated HBMECs. Scale bars 20 μm. ( B ) Analysis of the network parameter average vessel length shows a significant reduction with ATV treatment, both pre-tube formation and post (One-way ANOVA with Tukey’s post hoc multiple comparisons test ** P =0.003, *** P =0.0007, **** P <0.0001). ( C ) Cytotoxicity analysis of ATV treated tubes showed no difference from controls ( n =3, t -test).

Article Snippet: Primary human brain microvascular endothelial cells (HBMECs) (Innoprot P10361) were maintained on 1% gelatin coated flasks in endothelial cell growth medium MV (PromoCell C-22020).

Techniques:

Journal: bioRxiv

Article Title: Using atorvastatin-induced vascular weakness to model brain haemorrhage in vascularised cerebral organoids

doi: 10.64898/2026.04.20.719465

Figure Lengend Snippet: ( A ) Representative confocal images of whole organoids treated with ATV for 24 hours and the loss of VE-Cadherin expression from the surface. Scale bars 500 μm. ( B ) VE-Cadherin, not CD31 ( P =0.091), expressed as a percentage of DAPI was significantly reduced with ATV treatment compared to DMSO controls (two-tailed t -test, * P =0.011). ( C ) Size progression for 4 batches of organoids that were treated with ATV at day 40. ( D ) Vascular metrics were unchanged for CD31 ( n =15 organoids from 4 batches, non-significant t- test) with slightly more endpoints, signifying single cells. ( E ) Angiotool analysis of VE-Cadherin staining revealed shorter overall vessel length ( n =15 organoids from 4 batches, t- test, * P =0.0389)). ( F ) qPCR analysis of ATV-treated organoids showed a reduction in VE-Cadherin RNA expression; however, other markers of endothelial function are unchanged (One-Way ANOVA, n =5 organoids from 2 batches). ( G ) ATV treatment increased the expression of some cholesterol biosynthesis markers compared to DMSO controls, opposite to what was observed in HBMECs in 2D (One-Way ANOVA, n =5 organoids from 2 batches).

Article Snippet: Primary human brain microvascular endothelial cells (HBMECs) (Innoprot P10361) were maintained on 1% gelatin coated flasks in endothelial cell growth medium MV (PromoCell C-22020).

Techniques: Expressing, Two Tailed Test, Staining, RNA Expression

Journal: bioRxiv

Article Title: Glycan-coated nanoparticles mimicking the ischemic glycocalyx scavenge the complement system conferring protection after experimental ischemic stroke

doi: 10.64898/2026.03.30.715069

Figure Lengend Snippet: A ) The experimental plan for lectins binding to ihBMECs at the end of hypoxia or after re-oxygenation in absence/presence/. B ) Sensorgrams obtained with Quartz Crystal Microbalance showing the binding of ConA (upper panels) and WGA (lower) injected at four different concentration (0.7-2-6-18 µg/mL) over chip-adherent ihBMECs. The data show decreased binding at the end of the 16h of hypoxia and increased binding after the 4h of re-oxygenation either in presence or absence of MBL compared to normoxic ihBMECs. C ) Microphotographs of MBL (red) deposited on normoxic (left) or hypoxic (right) ihBMEC after re-oxygenation. Nuclei in blue (DAPI), scale bars 10 µm.

Article Snippet: Immortalized human brain microvascular endothelial cells (ihBMECs) (5000 cells/cm 2 ) (Innoprot) were seeded on black 96-well μ-plates (ibidi, Germany) with optically clear flat bottom, suitable for fluorescence microscopy.

Techniques: Binding Assay, Injection, Concentration Assay

Journal: bioRxiv

Article Title: Glycan-coated nanoparticles mimicking the ischemic glycocalyx scavenge the complement system conferring protection after experimental ischemic stroke

doi: 10.64898/2026.03.30.715069

Figure Lengend Snippet: A ) MBL detection on the soft and hard corona samples obtained after preincubation of GNPs with human serum. The MBL signal decreased in the soft corona concomitantly with the three washes (Soft C1-3) and no signal was captured in the fourth wash (Soft C.4). The presence of MBL in the Hard Corona (Hard C., i.e. the proteins remaining after the washings because of their high affinity for the GNPs,) was strong for Man-GNPs (black arrow), and much less for Glc-GNPs (white arrow). B ) The experimental plan for testing sugar-GNPs localization on ihBMEC. C ) 3D microphotographs of Man-GNPs (red, reflectance microscopy) and F-actin (phalloidin, green) in normoxic (CTRL) or hypoxic (HYP) ihBMECs undergone re-oxygenation in the presence of 40 µg/mL Man-GNPs in 30% human serum. Man-GNPs were internalized in the cytoplasm of ihBMECs. Nuclei in blue (DAPI), scale bar 10 µm. D ) Normoxic (CTRL) or hypoxic (HYPOXIA) ihBMECs undergone re-oxygenation in the presence of 5, 20 or 40 µg/mL Man-GNPs in 30% HS were analyzed by reflectance confocal microscopy for Man-GNPs and MBL co-localization. Microphotographs show that Man-GNPs (white, reflectance microscopy) and hMBL (red) did not co-localize (as seen in magnification of white frame, scale bar 1 µm). Phalloidin in green, nuclei in blue (DAPI), scale bar 10 µm.

Article Snippet: Immortalized human brain microvascular endothelial cells (ihBMECs) (5000 cells/cm 2 ) (Innoprot) were seeded on black 96-well μ-plates (ibidi, Germany) with optically clear flat bottom, suitable for fluorescence microscopy.

Techniques: Microscopy, Confocal Microscopy

Journal: bioRxiv

Article Title: Glycan-coated nanoparticles mimicking the ischemic glycocalyx scavenge the complement system conferring protection after experimental ischemic stroke

doi: 10.64898/2026.03.30.715069

Figure Lengend Snippet: A) Microphotographs of MBL (red) deposited on normoxic (CTRL) or hypoxic (HYPOXIA) ihBMECs undergone re-oxygenation in the presence of 5, 20 or 40 µg/mL Man-GNPs in 30% HS (w/Man-GNPs). Nuclei in blue (DAPI), scale bar 200 µm. B ) MBL deposition, measured as fluorescence intensity, was greater on hypoxic than normoxic cells exposed to 30% HS. This increase was significantly reduced when ihBMECs were exposed to 5 and 20 µg/mL of Man-GNPs. Data as mean with individual values ± SD (n= 4). Two-way ANOVA followed by Tukey’s multiple comparisons, **p<0.001, *p<0.05. C ) Overexpression of ICAM-1 in hypoxic ihBMECs was significantly reduced when the cells were exposed to 20 µg/mL of Man-GNPs, to a similar extent than exposure to MBL depleted HS 30% (Δ MBL). D ) Overexpression of MMP-2 in hypoxic ihBMECs was partially counteracted by 20 µg/mL of Man-GNPs. E ) Expression of IL-1α was not significantly changed in presence of Man-GNPs with or without hypoxia. Data from 3 independent experiments, presented as mean with individual values ± SD (n= 4-12). Two-way ANOVA followed by Tukey’s multiple comparisons, ****p<0.0001, ***p<0.001, **p<0.01, *p<0.05.

Article Snippet: Immortalized human brain microvascular endothelial cells (ihBMECs) (5000 cells/cm 2 ) (Innoprot) were seeded on black 96-well μ-plates (ibidi, Germany) with optically clear flat bottom, suitable for fluorescence microscopy.

Techniques: Fluorescence, Over Expression, Expressing

Journal: bioRxiv

Article Title: Glycan-coated nanoparticles mimicking the ischemic glycocalyx scavenge the complement system conferring protection after experimental ischemic stroke

doi: 10.64898/2026.03.30.715069

Figure Lengend Snippet: A) The experimental plan to generate ihBMECs’ normoxic or hypoxic conditioned medium (NORM CM, HYP CM, respectively) and co-cultures of hIPSC-derived neurons, astrocytes and microglia. B ) Microphotographs of GFAP (astrocytes, green), MAP-2 (neurons, red) exposed for 24h to NORM CM or HYP CM +/− Man-GNPs. White arrows point to damaged neurons, i.e. circular cells without dendrites. Nuclei in blue (DAPI), scale bar 10 µm. C ) The quantification of stained volumes (in µm 3 ) showed a decrease of MAP-2 volumes in co-cultures exposed to HYP CM, which was counteracted by Man-GNPs. Data as mean ± SD. Each value is a random field of view (FOV) selected automatically from the overview image. Two-way ANOVA for repeated measures followed by Sidak’s multiple comparisons, ****p<0.0001 (n= 16 FOVs from two experimental replicates, empty rectangles indicate the mean of each replicate). D ) Microphotographs of GFAP (green) and nuclei (DAPI, blue) with a yellow line along which we calculated the FWHM reported in the graph. Width of the first ramification emerging from astrocytic soma was calculated at gray level’s half maximum (HM) and was larger in HYP CM compared to NORM CM or HYP CM + Man-GNPs. Data as mean gray levels of 8 cells per group ± SEM. Two-way ANOVA followed by Tukey’s multiple comparisons, ***p<0.001. Scale bars 10 µm. E ) Microphotographs of GFAP (green), β3-tubulin (neurons, red) and Iba1 (microglia, purple) exposed for 24h to NORM CM or HYP CM +/− Man-GNPs. Dashed squares indicate the magnified views of microglia on the right panels. Nuclei in blue (DAPI), scale bar 100 µm in full images, 20 µm in magnifications. White traces in the magnifications correspond to the Iba1 skeletonized signal. F ) The quantification of microglia morphological parameters showed increased number of branches and junctions after HYP CM exposure, which was counteracted by Man-GNPs. Data as violin plot. Each dot is individual microglia. Kruskal-Wallis test, **p<0.01, ***p<0.001 (n= 25-40 cells from 3 FOVs placed in one well). G ) Histograms of frequency distributions of the morphological parameters in E, shown with automatically chosen bin size.

Article Snippet: Immortalized human brain microvascular endothelial cells (ihBMECs) (5000 cells/cm 2 ) (Innoprot) were seeded on black 96-well μ-plates (ibidi, Germany) with optically clear flat bottom, suitable for fluorescence microscopy.

Techniques: Derivative Assay, Staining

Journal: bioRxiv

Article Title: Single Cell Transcriptomics of Fibrotic Lungs Unveils Aging-associated Alterations in Endothelial and Epithelial Cell Regeneration

doi: 10.1101/2023.01.17.523179

Figure Lengend Snippet: (A) Volcano plots showing the distribution of differentially expressed genes in gCap EC clusters 1 and 2 compared to other gCap EC clusters. (B) Violin plots showing the expression genes enriched in cluster 1 and 2. (C) Heatmap showing average expression of glycolysis genes in quiescent (Q) versus activated (A) gCap EC clusters. (D, E) Ingenuity pathway analysis shows canonical pathways and upstream regulators enriched in clusters 1 and 2 relative to other gCap EC clusters. P values were generated in IPA using Fisher’s test (log2 FC ≤-0.1 or ≥0.1, p value ≤0.05). P value and activation z-score were used for plotting canonical pathways and activated upstream regulators respectively. (F, G) qPCR analyses of human lung microvascular ECs (HLMECs) treated with the LATS1/2 inhibitor TRULI and the siRNAs targeting YAP and TAZ for 48 hours. YAP activation in these cells partially recapitulates the gene expression signature observed in activated gCap ECs. Values are summarized as mean and SD and analyzed using a two-tailed Student’s t -test. (N = 3). (H) Immunofluorescence images showing genetically labeled gCap ECs (membrane-GFP) in uninjured lungs of Aplnr-CreER(T)-mTmG reporter mouse. Lungs from these mice were harvested ten days following the last dose of tamoxifen (five total doses). An antibody against the pan-endothelial cell marker PECAM-1 was used to visualize all lung ECs. PECAM-1 positive ECs from large vessels showed no GFP expression. (I) Schematic representation of the approach used to detect TrkB-expressing gCap ECs following bleomycin injury. gCap ECs (mGFP) were lineage labeled in Aplnr-CreER(T)-mTmG mice 15 days prior to bleomycin administration (Day 0). Sham and bleomycin-injured lungs were harvested 28 days post bleomycin delivery and subjected to immunofluorescence analysis. An antibody against TrkB was used to detect injured gCap ECs (Red). gCap ECs co-expressing GFP and TrkB (yellow) only emerged in injured lungs (n=2). (J). Immunofluorescence images showing TrkB-expressing cells in the lungs of young and aged mice 37 days post bleomycin challenge (n=2). (K) Schematic showing putative mechanisms implicated in of gCap EC remodeling in response to lung injury and during lung fibrosis resolution.

Article Snippet: Human lung microvascular endothelial cells (HLMECs) were purchased from Cell Applications (San Diego, CA, USA) or ANGIO-PROTEOMIE (Worcester, MA, USA) and maintained in endothelial cell growth basal medium supplemented with microvascular endothelial cell growth kit.

Techniques: Expressing, Generated, Activation Assay, Two Tailed Test, Immunofluorescence, Labeling, Marker

Journal: PLoS ONE

Article Title: CXCL12 Mediates Trophic Interactions between Endothelial and Tumor Cells in Glioblastoma

doi: 10.1371/journal.pone.0033005

Figure Lengend Snippet: ( A ) Human glioblastoma specimen immunostained for CXCL12 (brown) demonstrates expression in vascular endothelial cells. t = tumor cells, e = cross-section through tumor-associated capillary, and Scale bar = 25 µm. ( B ) HBMECs, in co-culture on Matrigel, express CXCL12 (red). Nuclei are counterstained blue with DAPI. Scale bar equals 25 µm. ( C ) Human brain micro-vascular endothelial cells cultured on Matrigel (Mat HBMEC) secrete CXCL12 into the media as determined by ELISA. Mat alone indicates results from Matrigel alone-conditioned media. N = 3. ** = p<0.005 as determined by two-tailed t -test. ( D ) Single cell suspensions from two different adult GBM patients (GBM1, GBM2) and cultured U87 cells express CXCR4 by western blotting. CXCR4 appears red and the actin loading control appears green.

Article Snippet: Primary human brain microvascular endothelial cells (HBMEC) were obtained from ScienCell, Carlsbad, CA).

Techniques: Expressing, Co-Culture Assay, Cell Culture, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Western Blot, Control

Journal: PLoS ONE

Article Title: CXCL12 Mediates Trophic Interactions between Endothelial and Tumor Cells in Glioblastoma

doi: 10.1371/journal.pone.0033005

Figure Lengend Snippet: ( A ) Twenty-four hours after establishing a capillary-like network of mcherry-expressing HBMECs in Matrigel, eGFP-expressing U87 cells were added to the culture. Within 24 hours U87 cells were seen in physical contact with HBMECs. Scale bar = 50 microns. ( B ) The mean distances between U87 cells (500 to 800 cells) and HBMECs were calculated at different time points after the addition of the tumor cells to the HBMEC networks. There was a significant increase in co-localization (reduction in mean distance) within 24 hrs, which was maintained over a 72 hr period. * = p<0.05 as determined by one way ANOVA for the means of three separate experiments involving 500–800 measurements per experiment. ( C ) The distance between approximately 1000 eGFP-expressing U87 cells and mCherry fluorescent protein-expressing HBMECs in co-culture (24 hrs) was measured and the distribution was plotted as the percentage of total cells in 20 micron increments (black triangles). More than 50% of the total U87 cells in the culture were within 40 microns of an endothelial cell. A theoretical plot of a random distribution of cells is shown (open circles). ( D ) The distance between GFAP positive GBM cells and mCherry fluorescent protein-expressing HBMECs in co-culture were measured and the distribution was plotted as the percentage of total cells in 20 micron increments (black triangles). Error bars represent SEM from three independent experiments involving three different GBM isolates. Approximately 500 GBM (GFAP positive) cells were counted. Nearly 80% of the GFAP positive GBM cells in the culture were within 20 microns of an endothelial cell. A theoretical plot of a random distribution of cells is shown (open circles).

Article Snippet: Primary human brain microvascular endothelial cells (HBMEC) were obtained from ScienCell, Carlsbad, CA).

Techniques: Expressing, Co-Culture Assay

Journal: Stem Cell Reviews and Reports

Article Title: Outgrowth Endothelial Cell Conditioned Medium Negates TNF-α-Evoked Cerebral Barrier Damage: A Reverse Translational Research to Explore Mechanisms

doi: 10.1007/s12015-022-10439-4

Figure Lengend Snippet: Schematic diagram of an in vitro model of human BBB and the effect of OEC-CM on BBB integrity and function and actin cytoskeleton organization in HBMECs and OECs. (A) In vitro models of human BBB consisting of astrocytes, pericytes, and HBMECs alone or mixed with OECs. (B, C) TNF-α significantly disrupted BBB integrity and function, as shown by decreases in TEER and concomitant increases in paracellular flux of sodium fluorescein, which were prevented by OEC-CM treatment. (D) Co-treatment with OEC-CM prevented the effects of TNF-α on cytoskeletal reorganization in HBMECs and OECs and decreased stress fiber formation (white arrows). (E) Quantification of stress fiber formation in both cells. Scale bar: 25 μm. * P < 0.05 versus BBB formed by HBMECs or control, # P < 0.05 versus BBB formed by HBMECs exposed to TNF-α, † P < 0.05 versus BBB formed by HBMECs exposed to TNF-α and OEC-CM, φ P < 0.05 versus BBB formed by HBMECs and OECs, ψ P < 0.05 versus BBB formed by HBMECs and OECs exposed to TNF-α (one-way ANOVA followed by Tukey's post-hoc analysis). BBB, blood–brain barrier; HBMECs, human brain microvascular endothelial cells; OEC-CM, outgrowth endothelial cell-derived conditioned medium; OECs, outgrowth endothelial cells; TNF-α, tumor necrosis factor-α

Article Snippet: Human brain microvascular endothelial cells (HBMECs), pericytes, and astrocytes were purchased from TCS CellWorks Ltd. (Buckingham, UK) and cultured at 37 °C in a humidified atmosphere (75% N 2 , 20% O 2 , 5% CO 2 ) with their respective media (Sciencell Research Laboratories, San Diego, USA).

Techniques: In Vitro, Control, Derivative Assay

Journal: Stem Cell Reviews and Reports

Article Title: Outgrowth Endothelial Cell Conditioned Medium Negates TNF-α-Evoked Cerebral Barrier Damage: A Reverse Translational Research to Explore Mechanisms

doi: 10.1007/s12015-022-10439-4

Figure Lengend Snippet: The effect of OEC-CM on HBMEC and OEC functional characteristics and analysis of angiogenesis-related proteins in HBMEC and OEC secretomes and OEC-CM. (A, B) OEC-CM accelerated wound closure in both HBMEC and OECs. (C-E) OEC-CM negated the impact of TNF-α on HBMEC and OEC tubule network. (F, G) Treatments with OEC-CM neutralized the inhibitory effect of TNF-α on HBMEC and OEC adhesion to fibronectin, an extracellular matrix protein. (H, I) Proteome profiling of OEC-CM along with HBMEC and OEC secretomes revealed significant variations in various pro- and anti-angiogenic factors e.g. endothelin-1, MCP-1 and endostatin in OEC-CM. Scale bars = 100 μm. * P < 0.05 versus control, # P < 0.05 versus TNF-α (one-way ANOVA followed by Tukey's post-hoc analysis). HBMECs, human brain microvascular endothelial cells; IL-8, interleukin-8; MCP-1, monocyte chemoattractant protein-1; OEC-CM, outgrowth endothelial cell-derived conditioned medium; OECs, outgrowth endothelial cells; TIMP-1, tissue inhibitors of metalloproteinase-1; TNF-α, tumor necrosis factor-α; uPA, urokinase plasminogen activator

Article Snippet: Human brain microvascular endothelial cells (HBMECs), pericytes, and astrocytes were purchased from TCS CellWorks Ltd. (Buckingham, UK) and cultured at 37 °C in a humidified atmosphere (75% N 2 , 20% O 2 , 5% CO 2 ) with their respective media (Sciencell Research Laboratories, San Diego, USA).

Techniques: Functional Assay, Control, Derivative Assay

Journal: BMC Microbiology

Article Title: Role of Mycobacterium tuberculosis pknD in the Pathogenesis of central nervous system tuberculosis

doi: 10.1186/1471-2180-12-7

Figure Lengend Snippet: Invasion and survival of M. tuberculosis pknD mutant in host-derived cells . A . BALB/c mice were infected with M. tuberculosis CDC1551 or pknD mutant, and sacrificed at days 1 and 49 after infection. The mutant for M. tuberculosis pknD was significantly attenuated (P = 0.004) in mouse brain, but not lung tissue, 49 days after infection. No defect was observed in the lungs at either time point. Bacterial burden is represented as log 10 CFU/organ for all animal experiments. B . Invasion of host-cell monolayers by wild-type CDC1551, wild-type intergenic transposon control, pknD transposon mutant (pknD:Tn), and pknD genetic complement (pknD:Comp) was examined and normalized to the wild-type control. Invasion assays were performed in brain microvascular endothelial cells (HBMEC), epithelial A549 cells, and umbilical vein endothelia (HUVEC). No difference in invasion was observed in A549 cells (P = 0.31) or HUVEC (P = 0.41). A significant reduction in invasive capacity, however, was observed in the CNS-derived HBMEC (P = 0.02). This defect was restored by genetic complementation with the native pknD/pstS2 operon. N.S. = not significantly different. C . Intracellular survival of each of the above M. tuberculosis strains was examined in HBMEC at days 1, 3, 5, and 7 after infection. The pknD:Tn mutant demonstrated an invasion and intracellular survival defect in HBMEC relative to wild-type over the course of the seven day infection. D . Survival was also examined by infection of activated J774 macrophages. No corresponding survival defect for the pknD:Tn mutant was observed in these cells during the seven day infection. A mutant for the gene Rv0442c , known to be attenuated in the macrophage model, is included as a control. All CFU counts are represented as mean ± standard deviation.

Article Snippet: Primary human brain microvascular endothelial cells and HUVEC were kind gifts from Dr. Kwang Sik Kim, Department of Pediatrics, Johns Hopkins University School of Medicine.

Techniques: Mutagenesis, Derivative Assay, Infection, Control, Standard Deviation

Journal: Molecular Pharmacology

Article Title: A Dietary Agonist of Transient Receptor Potential Cation Channel V3 Elicits Endothelium-Dependent Vasodilation S⃞

doi: 10.1124/mol.109.060715

Figure Lengend Snippet: Carvacrol stimulates TRPV3 cation currents in cerebral artery endothelial cells A, representative whole-cell currents recorded from human microvascular cerebral artery endothelial cells during voltage ramps from −100 to +100 mV. Current density is shown for cells under baseline conditions (B) and after first (1), second (2), and third (3) application of carvacrol (100 μM). B, summary data demonstrating sensitization of the carvacrol-induced current (n = 6). C, summary data showing the effects of the TRPA1 antagonist HC-030031 (HC, 3 μM) and the TRPV1–4 blocker RuR (10 μM) on carvacrol-induced currents recorded from cerebral artery endothelial cells; n = 5 for HC-030031, n = 4 for ruthenium red. Current magnitude was normalized to peak carvacrol-induced currents. *, P ≤ 0.05 versus control (C).

Article Snippet: Carvacrol-activated currents were recorded from human cerebral artery microvascular endothelial cells (Cell Systems Corporation, Kirkland, WA).

Techniques: Control