Journal: Molecular Medicine Reports

Article Title: X-irradiation induces acute and early term inflammatory responses in atherosclerosis-prone ApoE − / − mice and in endothelial cells

doi: 10.3892/mmr.2021.12038

Figure Lengend Snippet: Inflammatory response in endothelial cells at 24 h after irradiation. The response of various inflammatory markers at 24 h after 0.1 and 5 Gy irradiation is represented in (A-I) TICAE cells and (J-R) TIME cells, normalized to cell count. The Kruskal-Wallis test was used to analyse the data and the P-value was adjusted using the Benjamini-Hochberg method. Values represent the average ± SEM of 6 biological replicates. *P<0.05, **P<0.01 and ***P<0.001 vs. 0 Gy. p.i., post irradiation; GDF-15, growth differentiation factor-15; CXCL10, C-X-C motif chemokine ligand 10; ICAM-1, intercellular adhesion molecule-1; MCP-1, monocyte chemoattractant protein-1; uPAR, urokinase-type plasminogen activator receptor; PAI-1, plasminogen activator inhibitor-1; FGF-basic, basic fibroblast growth factor.

Article Snippet: In addition, TICAE cells, which are primary human coronary artery endothelial cells from the European Collection of Authenticated Cell Cultures (ECACC; HCAECs cat. no. 300-05a) that were transduced with retroviruses bearing the est2 gene, a yeast homologue of the human TERT protein ( , ), were used.

Techniques: Irradiation, Cell Counting

Journal: Molecular Medicine Reports

Article Title: X-irradiation induces acute and early term inflammatory responses in atherosclerosis-prone ApoE − / − mice and in endothelial cells

doi: 10.3892/mmr.2021.12038

Figure Lengend Snippet: Inflammatory response in endothelial cells at 72 h after irradiation. The response of various inflammatory markers at 72 h after 0.1 and 5 Gy irradiation is presented in (A-I) TICAE cells and (J-R) TIME cells. Data were normalized to cell count. The Kruskal-Wallis test was used to analyse the data and the P-value was adjusted using the Benjamini-Hochberg method. Values represent the average ± SEM of 6 biological replicates. *P<0.05, **P<0.01 and ***P<0.001 vs. 0 Gy. p.i., post irradiation; GDF-15, growth differentiation factor-15; CXCL10, C-X-C motif chemokine ligand 10; ICAM-1, intercellular adhesion molecule-1; MCP-1, monocyte chemoattractant protein-1; uPAR, urokinase-type plasminogen activator receptor; PAI-1, plasminogen activator inhibitor-1; FGF-basic, basic fibroblast growth factor.

Article Snippet: In addition, TICAE cells, which are primary human coronary artery endothelial cells from the European Collection of Authenticated Cell Cultures (ECACC; HCAECs cat. no. 300-05a) that were transduced with retroviruses bearing the est2 gene, a yeast homologue of the human TERT protein ( , ), were used.

Techniques: Irradiation, Cell Counting

Journal: Frontiers in Pharmacology

Article Title: Histamine Potentiates SARS-CoV-2 Spike Protein Entry Into Endothelial Cells

doi: 10.3389/fphar.2022.872736

Figure Lengend Snippet: Spike-induced ACE2 internalization is enhanced in the presence of histamine. (A) Representative Western blotting after surface biotinylation of intact endothelial cells with or without spike treatment for 30 min. (B) Mean data. (C) Representative Western blot after surface biotinylation showing that increased incubation time after spike treatment induced ACE2 internalization and degradation. (D) Mean data. * p < 0.05 vs . surface band intensity of the untreated control. (E) Representative Western blot after surface biotinylation showing the effect of bafilomycin A1 on spike-induced ACE2 degradation. (F) Mean data, * p < 0.05 vs . untreated, # p < 0.05 vs . spike treated. (G) Representative Western blot after surface biotinylation showing that histamine potentiates spike-induced ACE2 internalization within 30 min of treatment. (H) Mean data, * p < 0.05 vs . surface band intensity of untreated control. n = 4 for all the experimental sets. I- indicates intracellular fraction, S-denotes surface or plasma membrane fraction.

Article Snippet: The human primary coronary artery endothelial cells were purchased from Cell Biologics Inc.

Techniques: Western Blot, Incubation, Control, Clinical Proteomics, Membrane

Journal: Frontiers in Pharmacology

Article Title: Histamine Potentiates SARS-CoV-2 Spike Protein Entry Into Endothelial Cells

doi: 10.3389/fphar.2022.872736

Figure Lengend Snippet: Histamine H2 receptor signaling is involved in histamine potentiating spike–ACE2 internalization. (A) Representative Western blot after surface biotinylation of the intact endothelial cells showing the effect of famotidine on the potentiating effect of histamine on spike-ACE2 internalization. (B) Mean data. (C) Representative Western blot after surface biotinylation showing the effect of the protein kinase A inhibitor, PKI, in preventing histamine-induced spike–ACE2 internalization. (D) Mean data. * p < 0.05 vs . the untreated control, # p < 0.05 vs . spike + histamine. (E) Representative Western blot after surface biotinylation showing the effect of H2 receptor protein knockdown on spike + histamine treatment. Scrm-scrambled siRNA. (F) Mean data. * p < 0.05 vs . untreated control, # p < 0.05 vs . spike + histamine scrambled control. n = 4 for all the experimental sets. I- indicates intracellular fraction, S-denotes surface or plasma membrane fraction.

Article Snippet: The human primary coronary artery endothelial cells were purchased from Cell Biologics Inc.

Techniques: Western Blot, Control, Knockdown, Clinical Proteomics, Membrane