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Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells

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Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells. / Barroso, M; Rocha, Monica S; Esse, Ruben; Gonçalves, I; Gomes, A Q; Teerlink, Tom; Jakobs, C; Blom, Henk J; Loscalzo, Joseph; Rivera, Isabel; de Almeida, I Tavares; Castro, Rita.

in: AMINO ACIDS, Jahrgang 42, Nr. 5, 05.2012, S. 1903-11.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Barroso, M, Rocha, MS, Esse, R, Gonçalves, I, Gomes, AQ, Teerlink, T, Jakobs, C, Blom, HJ, Loscalzo, J, Rivera, I, de Almeida, IT & Castro, R 2012, 'Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells', AMINO ACIDS, Jg. 42, Nr. 5, S. 1903-11. https://doi.org/10.1007/s00726-011-0916-0

APA

Barroso, M., Rocha, M. S., Esse, R., Gonçalves, I., Gomes, A. Q., Teerlink, T., Jakobs, C., Blom, H. J., Loscalzo, J., Rivera, I., de Almeida, I. T., & Castro, R. (2012). Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells. AMINO ACIDS, 42(5), 1903-11. https://doi.org/10.1007/s00726-011-0916-0

Vancouver

Barroso M, Rocha MS, Esse R, Gonçalves I, Gomes AQ, Teerlink T et al. Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells. AMINO ACIDS. 2012 Mai;42(5):1903-11. https://doi.org/10.1007/s00726-011-0916-0

Bibtex

@article{d45f58c73e934aae9a6d04ea742fbf01,
title = "Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells",
abstract = "Hyperhomocysteinemia (HHcy) is a risk factor for vascular disease, but the underlying mechanisms remain incompletely defined. Reduced bioavailability of nitric oxide (NO) is a principal manifestation of underlying endothelial dysfunction, which is an initial event in vascular disease. Inhibition of cellular methylation reactions by S-adenosylhomocysteine (AdoHcy), which accumulates during HHcy, has been suggested to contribute to vascular dysfunction. However, thus far, the effect of intracellular AdoHcy accumulation on NO bioavailability has not yet been fully substantiated by experimental evidence. The present study was carried out to evaluate whether disturbances in cellular methylation status affect NO production by cultured human endothelial cells. Here, we show that a hypomethylating environment, induced by the accumulation of AdoHcy, impairs NO production. Consistent with this finding, we observed decreased eNOS expression and activity, but, by contrast, enhanced NOS3 transcription. Taken together, our data support the existence of regulatory post-transcriptional mechanisms modulated by cellular methylation potential leading to impaired NO production by cultured human endothelial cells. As such, our conclusions may have implications for the HHcy-mediated reductions in NO bioavailability and endothelial dysfunction.",
keywords = "Arginine, Cells, Cultured, Endothelial Cells, Gene Expression Regulation, Human Umbilical Vein Endothelial Cells, Humans, Hyperhomocysteinemia, Methylation, Nitric Oxide, Nitric Oxide Synthase Type III, S-Adenosylhomocysteine, Vascular Diseases, Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't",
author = "M Barroso and Rocha, {Monica S} and Ruben Esse and I Gon{\c c}alves and Gomes, {A Q} and Tom Teerlink and C Jakobs and Blom, {Henk J} and Joseph Loscalzo and Isabel Rivera and {de Almeida}, {I Tavares} and Rita Castro",
year = "2012",
month = may,
doi = "10.1007/s00726-011-0916-0",
language = "English",
volume = "42",
pages = "1903--11",
journal = "AMINO ACIDS",
issn = "0939-4451",
publisher = "Springer Wien",
number = "5",

}

RIS

TY - JOUR

T1 - Cellular hypomethylation is associated with impaired nitric oxide production by cultured human endothelial cells

AU - Barroso, M

AU - Rocha, Monica S

AU - Esse, Ruben

AU - Gonçalves, I

AU - Gomes, A Q

AU - Teerlink, Tom

AU - Jakobs, C

AU - Blom, Henk J

AU - Loscalzo, Joseph

AU - Rivera, Isabel

AU - de Almeida, I Tavares

AU - Castro, Rita

PY - 2012/5

Y1 - 2012/5

N2 - Hyperhomocysteinemia (HHcy) is a risk factor for vascular disease, but the underlying mechanisms remain incompletely defined. Reduced bioavailability of nitric oxide (NO) is a principal manifestation of underlying endothelial dysfunction, which is an initial event in vascular disease. Inhibition of cellular methylation reactions by S-adenosylhomocysteine (AdoHcy), which accumulates during HHcy, has been suggested to contribute to vascular dysfunction. However, thus far, the effect of intracellular AdoHcy accumulation on NO bioavailability has not yet been fully substantiated by experimental evidence. The present study was carried out to evaluate whether disturbances in cellular methylation status affect NO production by cultured human endothelial cells. Here, we show that a hypomethylating environment, induced by the accumulation of AdoHcy, impairs NO production. Consistent with this finding, we observed decreased eNOS expression and activity, but, by contrast, enhanced NOS3 transcription. Taken together, our data support the existence of regulatory post-transcriptional mechanisms modulated by cellular methylation potential leading to impaired NO production by cultured human endothelial cells. As such, our conclusions may have implications for the HHcy-mediated reductions in NO bioavailability and endothelial dysfunction.

AB - Hyperhomocysteinemia (HHcy) is a risk factor for vascular disease, but the underlying mechanisms remain incompletely defined. Reduced bioavailability of nitric oxide (NO) is a principal manifestation of underlying endothelial dysfunction, which is an initial event in vascular disease. Inhibition of cellular methylation reactions by S-adenosylhomocysteine (AdoHcy), which accumulates during HHcy, has been suggested to contribute to vascular dysfunction. However, thus far, the effect of intracellular AdoHcy accumulation on NO bioavailability has not yet been fully substantiated by experimental evidence. The present study was carried out to evaluate whether disturbances in cellular methylation status affect NO production by cultured human endothelial cells. Here, we show that a hypomethylating environment, induced by the accumulation of AdoHcy, impairs NO production. Consistent with this finding, we observed decreased eNOS expression and activity, but, by contrast, enhanced NOS3 transcription. Taken together, our data support the existence of regulatory post-transcriptional mechanisms modulated by cellular methylation potential leading to impaired NO production by cultured human endothelial cells. As such, our conclusions may have implications for the HHcy-mediated reductions in NO bioavailability and endothelial dysfunction.

KW - Arginine

KW - Cells, Cultured

KW - Endothelial Cells

KW - Gene Expression Regulation

KW - Human Umbilical Vein Endothelial Cells

KW - Humans

KW - Hyperhomocysteinemia

KW - Methylation

KW - Nitric Oxide

KW - Nitric Oxide Synthase Type III

KW - S-Adenosylhomocysteine

KW - Vascular Diseases

KW - Journal Article

KW - Research Support, N.I.H., Extramural

KW - Research Support, Non-U.S. Gov't

U2 - 10.1007/s00726-011-0916-0

DO - 10.1007/s00726-011-0916-0

M3 - SCORING: Journal article

C2 - 21614558

VL - 42

SP - 1903

EP - 1911

JO - AMINO ACIDS

JF - AMINO ACIDS

SN - 0939-4451

IS - 5

ER -