Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Glutamate Exacerbates Traumatic Brain Injury‐Induced Acute Lung Injury Through NMDAR / ROS /Ca 2+ Signaling Pathway in Pulmonary Endothelial Cells

doi: 10.1002/kjm2.70087

Figure Lengend Snippet: Changes of serious lung injury after TBI‐ALI. (A) The TTC staining was performed to evaluate the brain injury volume. (B) The level of cytokines (TNF‐α, IL‐1β, and IL‐6) in peripheral blood. (C) The level of cytokines (TNF‐α, IL‐1β, and IL‐6) in BALF. (D, E) The wet/dry weight ratio and the protein concentration are detected. (F, G) Corresponding lung H&E staining and acute lung injury scores. (H) The expression of GluN1 in HPMVECs. Scale bar, 200 μm. Results represent the mean ± SEM of independent experiments of animals ( n = 8). * p < 0.05 versus Sham group; # p < 0.05 versus TBI group.

Article Snippet: Human pulmonary microvascular endothelial cells (HPMVECs) were purchased from Cell Applications Inc. (San Diego, CA, USA; Catalog No. 300K‐05a) and cultured in RPMI‐1640 medium (Thermo Fisher Scientific, Waltham, MA, USA) with 1% penicillin–streptomycin and 10% fetal bovine serum (FBS, Gbico, Grand Island, NY, USA) at 37°C in a humidified atmosphere containing 5% CO 2 .

Techniques: Staining, Protein Concentration, Expressing

Journal: The Kaohsiung Journal of Medical Sciences

Article Title: Glutamate Exacerbates Traumatic Brain Injury‐Induced Acute Lung Injury Through NMDAR / ROS /Ca 2+ Signaling Pathway in Pulmonary Endothelial Cells

doi: 10.1002/kjm2.70087

Figure Lengend Snippet: Glutamate alters NMDAR/ROS/Ca 2+ pathway. (A) Cell viability (percentage of untreated control) of HPMVECs after the treatment of glutamate. (B) Immunofluorescence images showing ROS production in HPMVECs. (C) Comparison of Ca 2+ concentration in each group. (D) The levels of p‐NFAT and p‐p65 in cytoplasm and nucleus were tested by western blot. (E) Immunofluorescence stain of p‐NFAT and p‐p65 in nucleus. Results represent the mean ± SEM of independent experiments of cells ( n = 3). * p < 0.05 versus Sham group; # p < 0.05 versus Glu group.

Article Snippet: Human pulmonary microvascular endothelial cells (HPMVECs) were purchased from Cell Applications Inc. (San Diego, CA, USA; Catalog No. 300K‐05a) and cultured in RPMI‐1640 medium (Thermo Fisher Scientific, Waltham, MA, USA) with 1% penicillin–streptomycin and 10% fetal bovine serum (FBS, Gbico, Grand Island, NY, USA) at 37°C in a humidified atmosphere containing 5% CO 2 .

Techniques: Control, Immunofluorescence, Comparison, Concentration Assay, Western Blot, Staining

Journal: ACS applied materials & interfaces

Article Title: Extracellular Vesicles Enhance the Remodeling of Cell-Free Silk Vascular Scaffolds in Rat Aortae.

doi: 10.1021/acsami.0c06609

Figure Lengend Snippet: Figure 2: A: Proliferation and B: migration of smooth muscle cells (SMCs) and endothelial cells (ECs) when exposed to extracellular vesicle (EV) based treatments. BM: Basal media; PBS: Phosphate buffered saline; EV50: 50 μl of EV isolate; EV150: 150 μl of EV isolate; SBM: Supplemented basal media. * represents p < 0.05, ** represents p < 0.005 and *** represents p < 0.0001.

Article Snippet: 22 Human coronary artery endothelial cells (ECs) were obtained from Cell Applications 23 (#300-05a), cultured in supplemented basal media (#212K-500, Cell Applications 24 Inc, SBM) and used at passage 4.

Techniques: Migration, Saline

Journal: Virulence

Article Title: PepO and CppA modulate Streptococcus sanguinis susceptibility to complement immunity and virulence

doi: 10.1080/21505594.2023.2239519

Figure Lengend Snippet: Contribution of pepO and cppA to the S. sanguinis capacity to invade human coronary artery endothelial cells. Bacterial invasion into primary HCAEC was determined in antibiotic-protection assays with pepO and cppA mutants, SK36 and complemented strains (+). Strains were treated with human serum (HS) (a,b), heat-inactivated serum (HIS) (c,d) or PBS (e,f) before co-cultivation with HCAEC. Invasion rates were expressed as the percentage of intracellular bacteria in relation to the initial inoculum. Columns represent means of three independent experiments. Bars indicate standard deviation values. Asterisks indicate significant differences in relation to SK36 (Kruskal-Wallis with post hoc Dunn’s test; * p < 0.05).

Article Snippet: Briefly, primary HCAEC (Lonza) were cultured in basal medium (EBM-2, Lonza) supplemented with EGM-2 MV (Lonza) and seeded (1 × 10 5 cells/well) in 24-well culture plates (Corning).

Techniques: Bacteria, Standard Deviation

Journal: Diabetes & Vascular Disease Research

Article Title: Mitochondrial mitophagy protection combining rivaroxaban and aspirin in high glucose-exposed human coronary artery endothelial cell. An in vitro study

doi: 10.1177/14791641221129877

Figure Lengend Snippet: Panel a.- Representative Western-blot of the Factor Xa (FXA) expression in human coronary artery endothelial cells (HCAEC) incubated with normal D-glucose concentration (5mmol/L, control) and in the presence of 30 mmol/L D-Glucose (+Glucose). Panel b.- Representative Western-blot of tissue factor (TF) expression in HCAEC incubated with normal D-glucose concentration (5 mmol/L, control) or with high glucose, 30 mmol/L D-Glucose (+Glucose). Experiments adding 50 nmol/L Rivaroxaban, 0.33 mmol/L ASA and 12.5 nmol/L Rivaroxaban +0.33 mmol/L ASA to high D-glucose-incubated HCAEC are also represented. Panel c.- Representative dot-blots to measure mitochondrial content of Pink-1 and Parkin proteins HCAEC incubated with 5 mmol/L D- (control) or 30 mmol/L D-Glucose (+Glucose). Experiments adding 50 nmol/L Rivaroxaban, 0.33 mmol/L ASA and 12.5 nmol/L Rivaroxaban +0.33 mmol/L ASA to high D-glucose-incubated HCAEC are also represented. Panel d.- Reactive oxygen species (ROS) production and changes in mitochondria membrane potential (ΔΨm) in HCAEC incubated with 5 mmol/L D- (control) or 30 mmol/L D-Glucose (+Glucose). Experiments adding 50 nmol/L Rivaroxaban, 0.33 mmol/L ASA and 12.5 nmol/L Rivaroxaban +0.33 mmol/L ASA to high D-glucose-incubated HCAEC are also represented. All experiments were also performed in presence of submaximal thrombin concentration (0.025 U/mL). Bar graphs of the four panels show the densitometric analysis represented in arbitrary units (A.U.). Results are represented as mean ± SEM of six different experiments. * p < 0.05 compared to the experiments performed normal glucose (5 mmol/L, control). # p < 0.05 compared to the experiments performed with 30 mmol/L glucose (+Glucose).

Article Snippet: The human coronary artery endothelial cell (HCAEC) line, (Ref. 350–05a, Merck KGaA, Germany) was incubated under the following experimental conditions: HCAEC incubated with physiologic D-glucose concentration (5 mmol/L, control group), HCAEC incubated with 30 mmol/L D-Glucose to mimic an hyperglycemic condition (+Glucose group), HCAEC incubated with 30 mmol/L D-Glucose+50 nmol/L Rivaroxaban (Bay 59–7939, Rivaroxaban group), HCAEC incubated with 30 mmol/L D-Glucose+0.33 mmol/L acetylsalicylic acid (ASA group) and 30 mmol/L D-glucose incubated HCAEC with Rivaroxaban (12.5 nmol/L) +ASA (0.33 mmol/L) (Riva+ASA group).

Techniques: Western Blot, Expressing, Incubation, Concentration Assay