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(Circulation Research. 2000;86:e50.)
© 2000 American Heart Association, Inc.

UltraRapid Communications

Regulation of Endothelial Nitric Oxide Synthase Expression by Albumin-Derived Advanced Glycosylation End Products

Armando Rojas, Sheyla Romay, Deyarina González, Beatriz Herrera, Rene Delgado, Karel Otero

From the Laboratorio de Farmacología (A.R., D.G., B.H., R.D., K.O.), Centro de Química Farmacéutica, Apartado Postal 6990, La Habana, Cuba; Laboratorio de Bioquímica (S.R.), Centro Nacional de Investigaciones Científicas, Apartado Postal 6880, La Habana, Cuba.

Correspondence to Armando Rojas, Centro de Química Farmacéutica, Ave 21 esquina a 200, Apartado Postal 6990, La Habana, Cuba. E-mail ily{at}biocnic.cneuro.edu.cu

Abstract—We examined whether albumin-derived advanced glycosylation end products (AGEs) downregulate the expression of endothelial nitric oxide synthase (NOS). Significant reductions in NOS activity and cGMP levels in bovine aortic endothelial cells were observed when exposed to different concentrations of albumin-derived AGEs. Western and Northern blot analyses showed significant decreases at the protein and transcript levels. Both reductions became evident after 24 hours of exposure. Nuclear run-on assays showed that AGE-BSA did not modify the transcription rate of the NOS III gene; however, AGE-BSA treatment markedly reduced the half-life of NOS III mRNA. In addition, AGE-treated endothelial cells displayed significant reduction on their antiplatelet properties. These results indicate that NOS expression is reduced by AGEs by increasing the rate of mRNA degradation and may be relevant to the impairment of some endothelial functions observed in diabetes and aging. The full text of this article is available at http://www.circresaha.org.

Key Words: advanced glycosylation end products • nitric oxide synthase • diabetes

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