eNOS, Nitric Oxide Signaling, and Endothelial Function
Endothelial nitric oxide synthase (eNOS), encoded by NOS3, is the primary source of nitric oxide (NO) in the vascular endothelium. NO produced by eNOS regulates vascular tone, endothelial permeability, platelet activation, leukocyte adhesion, angiogenesis, and the inflammatory state of the vessel wall.
Impaired NO bioavailability is a defining feature of endothelial dysfunction and has been associated with atherosclerosis, hypertension, coronary artery disease, metabolic disease, and vascular aging. Because eNOS regulates multiple endothelial functions, NOS3 genotype can be relevant to a broad range of vascular biology assays — including angiogenesis, migration, permeability, oxidative stress, and inflammatory signaling.
Neither variant alone determines cardiovascular disease outcome. Effects are probabilistic and interact with other genetic and environmental factors.
Confirmed Genotypes in Aortic and Coronary Artery Endothelial Cells
| Cell Type | Catalog No. | rs1799983 (Glu298Asp) | rs2070744 (-786T>C) |
|---|---|---|---|
| Human Aortic Endothelial Cells | Cat. #6100 | GG (WT) TT (Hom Var) | TT (WT) CT (Het) CC (Hom Var) |
| Human Coronary Artery Endothelial Cells | Cat. #6020 | GG (WT) GT (Het) TT (Hom Var) | TT (WT) CT (Het) |
Control NOS3 Genotype as an Experimental Variable
Primary endothelial cells from donors of unknown NOS3 genotype carry uncharacterized variation at these loci — variation that influences baseline eNOS expression, NO production, and responses to experimental stimuli. Immortalized endothelial lines offer reproducibility but may not faithfully reflect primary human eNOS biology. iPSC-derived and CRISPR-edited models allow isolation of individual variants but lack the broader native donor genetic background.
Control NOS3 genotype as an experimental variable
Select coding or promoter variant status as part of study design rather than accepting unknown donor backgrounds.
Compare eNOS expression and activity
Contrast rs1799983 wild-type and variant backgrounds in endothelial function assays with defined genetic context.
Separate regulatory from coding effects
Independently study rs1799983 (protein function) and rs2070744 (expression level) contributions to eNOS-dependent phenotypes.
Investigate genotype-dependent drug responses
Screen cardiovascular compounds across defined NOS3 genetic backgrounds to identify pharmacogenomic differences.
Reduce variability in standard endothelial assays
Angiogenesis, migration, permeability, and NO production assays all benefit from controlled NOS3 genotype background.
Access vascular bed–specific models
Aortic and coronary artery endothelial cells provide vessel-specific biology relevant to the research area — general vs. coronary vascular disease modeling.
Applications Specific to NOS3 Endothelial Biology
Requesting NOS3 Genotype-Defined Lots
Genotype-defined lots are available by request. Each lot ships with a COA confirming genotype at both NOS3 loci. A selection and verification fee applies per vial.
Identify the Cell Type
Identify the endothelial cell type — aortic (Cat. #6100) or coronary artery (Cat. #6020)
Specify NOS3 Genotype
Specify the NOS3 variant(s) and genotype(s) required — coding variant (rs1799983), promoter variant (rs2070744), or both.
Submit Your Request
Our team will confirm available lots and recommend the right genotype configuration for your study design
Please note that availability varies by genotype and donor lot. A selection and verification fee will be applied per vial and reflected in your quote.
For information on available genotypes, assistance selecting the right cells, or inquiries about additional genotypes and cell types, please contact us at info@sciencellonline.com, or call 1.877.602.8549.