Journal: Clinical Immunology (Orlando, Fla.)

Article Title: SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts

doi: 10.1016/j.clim.2021.108733

Figure Lengend Snippet: Adventitial fibroblast viability (A), density (B) and metabolic activity (C) after the exposure to SARS-CoV-2 Spike (S) Protein, Nucleocapsid (N) Protein and Membrane-Envelope (M) Protein for 24 h (A and B) or 1 h (C). All data are reported as the mean + standard error of the mean for 9 independent experiments (for viability/density) and 3 independent experiments (for metabolic activity). *Significantly different than negative control (ANOVA, Duncan method).

Article Snippet: Human aortic adventitial fibroblasts (AFs) were purchased from ScienCell Research Laboratories (Carlsbad, CA) and maintained in fibroblast medium-2 supplemented with 5% fetal bovine serum, antibiotics (penicillin/streptomycin) and growth supplement (as suggested by the manufacturer) at 37 °C and 5% CO 2 .

Techniques: Activity Assay, Membrane, Negative Control

Journal: Clinical Immunology (Orlando, Fla.)

Article Title: SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts

doi: 10.1016/j.clim.2021.108733

Figure Lengend Snippet: gC1qR expression on the cell membrane of adventitial fibroblasts after exposure to SARS-CoV-2 Spike (S) Protein, Nucleocapsid (N) Protein and Membrane-Envelope (M) Protein for 1 h. We observed different protein locations that are associated with different structural and functional locations of gC1qR: including 60.11 (A, the C1q globular head binding domain), 74.5.2 (B, activation of kinin and coagulation systems) and 83.13 (C, the HK binding domain). All data are reported as the mean + standard error of the mean for a minimum of 4 independent experiments (range 4–14). *Significantly different than negative control (ANOVA, Duncan method).

Article Snippet: Human aortic adventitial fibroblasts (AFs) were purchased from ScienCell Research Laboratories (Carlsbad, CA) and maintained in fibroblast medium-2 supplemented with 5% fetal bovine serum, antibiotics (penicillin/streptomycin) and growth supplement (as suggested by the manufacturer) at 37 °C and 5% CO 2 .

Techniques: Expressing, Membrane, Functional Assay, Binding Assay, Activation Assay, Coagulation, Negative Control

Journal: Clinical Immunology (Orlando, Fla.)

Article Title: SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts

doi: 10.1016/j.clim.2021.108733

Figure Lengend Snippet: ICAM-1 (A), Tissue Factor (B), RAGE (C) and GLUT-4 (D) expression on the cell membrane of adventitial fibroblasts after exposure to SARS-CoV-2 Spike (S) Protein, Nucleocapsid (N) Protein and Membrane-Envelope (M) Protein for 1 h. All data are reported as the mean + standard error of the mean for a minimum of 4 independent experiments (range 4–5 for ICAM-1, 7 for tissue factor, 6–7 for RAGE and 6–7 for GLUT-4). *Significantly different than negative control (ANOVA, Duncan method).

Article Snippet: Human aortic adventitial fibroblasts (AFs) were purchased from ScienCell Research Laboratories (Carlsbad, CA) and maintained in fibroblast medium-2 supplemented with 5% fetal bovine serum, antibiotics (penicillin/streptomycin) and growth supplement (as suggested by the manufacturer) at 37 °C and 5% CO 2 .

Techniques: Expressing, Membrane, Negative Control

Journal: Clinical Immunology (Orlando, Fla.)

Article Title: SARS-CoV-2 proteins regulate inflammatory, thrombotic and diabetic responses in human arterial fibroblasts

doi: 10.1016/j.clim.2021.108733

Figure Lengend Snippet: Proposed model of SARS-CoV-2 structural protein induced adventitial fibroblast inflammation, thrombosis, and diabetes progression. SARS-CoV-2 that has entered the vasculature can localize to the endothelium via gC1qR or transmigrate into the sub-endothelial space where viral structural proteins (Spike, Nucleocapsid, Membrane and/or Envelope Proteins) can interact with adventitial fibroblast gC1qR. The interaction of SARS-CoV-2 structural proteins with fibroblast gC1qR may activate internal signal transduction pathways (such as the MAPK pathway), which can lead to the enhanced expression or activation of GLUT-4, RAGE (receptor for advanced glycation end products), tissue factor, ICAM-1, and gC1qR's high molecular weight kininogen (HK) binding site. As each of these receptors interact with their specific ligands, vascular responses such as hypoglycemia, chronic inflammation, edema, coagulation, and thrombosis may be observed or promoted leading to vascular dysfunction. Further, each of these receptors and their heightened responses have been implicated in vascular disease progression. Importantly, these vascular disease responses have been shown to be heightened during COVID-19 progression, thus this figure proposes a possible mechanism to link SARS-CoV-2 infection and vascular disease progression.

Article Snippet: Human aortic adventitial fibroblasts (AFs) were purchased from ScienCell Research Laboratories (Carlsbad, CA) and maintained in fibroblast medium-2 supplemented with 5% fetal bovine serum, antibiotics (penicillin/streptomycin) and growth supplement (as suggested by the manufacturer) at 37 °C and 5% CO 2 .

Techniques: Membrane, Transduction, Expressing, Activation Assay, High Molecular Weight, Binding Assay, Coagulation, Biomarker Discovery, Infection

Journal: Circulation

Article Title: Loss of Cardio-Protective Effects at the ADAMTS7 Locus Due to Gene-Smoking Interactions

doi: 10.1161/CIRCULATIONAHA.116.022069

Figure Lengend Snippet: Genome browser view of regulatory features at rs7178051 on Chr15q21.1. ChIP-seq experiments were performed on confluent HCASMC for TCF21, Jun, JunD, CEBP and H3K4me1, H3K27me3, H3K27ac. DNAaseI hypersensitivity data for human AoSMC were acquired from the ENCODE project. Human aortic tissue H3K4me1, H3K9me3, H3K27me3, and H3K36me3 ChIP-seq data were acquired from the NIH Roadmap Epigenomics Project. HCASMC = human coronary artery smooth muscle cells; AoSMC = human aortic smooth muscle cells.

Article Snippet: ADAMTS7 and CHRNB4-A3-A5 mRNA levels were measured in cultured human coronary artery smooth muscle cells (HCASMC; Lonza CC-2583, Lonza Walkersville, MD), human coronary artery endothelial cells (HCAEC, Lonza CC-2585), human aortic smooth muscle cells (HAoSMC, Lonza CC-2571), human aortic endothelial cells (HAoEC, Lonza CC-2535), human aortic adventitial fibroblasts (HAoAF, Lonza CC-7014), and human acute monocytic leukemia cell line (THP-1, ATCC TIB-202).

Techniques: ChIP-sequencing