Publication:
Effects of human endothelial gene polymorphisms on cellular responses to hyperglycaemia: Role of NOS3 (Glu298Asp) and ACE (I/D) polymorphisms

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Issued Date

2011

Resource Type

Article

File Type

application/pdf

ISSN

14791641

DOI

10.1177/1479164111416679

Other identifier(s)

2-s2.0-80053058309

Rights Holder(s)

มหาวิทยาลัยศรีนครินทรวิโรฒ

Bibliographic Citation

Diabetes and Vascular Disease Research. Vol 8, No.4 (2011), p.276-283

Suggested Citation

Joshi M.S., Wattanapitayakul S., Schanbacher B.L., Bauer J.A. Effects of human endothelial gene polymorphisms on cellular responses to hyperglycaemia: Role of NOS3 (Glu298Asp) and ACE (I/D) polymorphisms. Diabetes and Vascular Disease Research. Vol 8, No.4 (2011), p.276-283. doi:10.1177/1479164111416679 Retrieved from: https://hdl.handle.net/20.500.14740/7234

Title

Effects of human endothelial gene polymorphisms on cellular responses to hyperglycaemia: Role of NOS3 (Glu298Asp) and ACE (I/D) polymorphisms

Author(s)

Joshi M.S.
 Wattanapitayakul S.
 Schanbacher B.L.
 Bauer J.A.

Abstract

The functional relevance of NOS3 and ACE genetic variations to endothelial cell function is largely unstudied. Here we tested the functional relevance of the NOS3 (Glu298Asp) polymorphism and ACE (I/D) polymorphism in endothelial cells in vitro. Our hypothesis was that these genetic polymorphisms alter endothelial cell sensitivity to glucose and 3-nitrotyrosine (3NT). Genotyped HUVECs were incubated with glucose, free 3NT or a combination of these two toxicants. Significant differences in glucose-induced cell death and free 3NT-induced cell death were observed among the NOS3 genotypes. Combined glucose/3NT caused increased toxicity among the NOS3 genotypes. No differences were observed among the ACE genotypes in their responses to glucose/3NT. These data demonstrate that the NOS3 genotype may be an important predictor of, or be mechanistically involved in, endothelial vulnerability, whereas the ACE I/D genotype is apparently less important. Thus this NOS3 genetic variation may play a role in vulnerability to endothelium-dependent diabetic vascular complications. © SAGE Publications 2011.

Subject(s)

3 nitrotyrosine
 Dipeptidyl carboxypeptidase
 Endothelial nitric oxide synthase
 Glucose
 Article
 Cell death
 Cell viability
 Cellular stress response
 Genetic polymorphism
 Genetic variability
 Genotype
 Human
 Human cell
 Human cell culture
 Hyperglycemia
 In vitro study
 Umbilical vein endothelial cell
 Caveolin 1
 Cell Death
 Cells, Cultured
 Diabetic Angiopathies
 Genotype
 Glucose
 Human Umbilical Vein Endothelial Cells
 Humans
 Hyperglycemia
 Nitric Oxide Synthase Type III
 Nitrites
 Peptidyl-Dipeptidase A
 Phenotype
 Phosphorylation
 Polymorphism, Genetic
 Proto-Oncogene Proteins c-akt
 Tyrosine

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URI

https://hdl.handle.net/20.500.14740/7234

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Scopus: Year 1983-2021

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