Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I overexpression.

Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I overexpression.

Εμφάνιση άλλων εκδόσεων (1)

Increased production of reactive oxygen species and loss of endothelial NO bioactivity are key features of vascular disease states such as diabetes mellitus. Tetrahydrobiopterin (BH4) is a required cofactor for eNOS activity; pharmacologic studies suggest that BH4 may mediate some of the adverse eff...

Πλήρης περιγραφή

Λεπτομέρειες βιβλιογραφικής εγγραφής
Κύριοι συγγραφείς:	Alp, N, Mussa, S, Khoo, J, Cai, S, Guzik, T, Jefferson, A, Goh, N, Rockett, K, Channon, K
Μορφή:	Journal article
Γλώσσα:	English
Έκδοση:	2003

Παρόμοια τεκμήρια

Nitric oxide Bioavailability is preserved in diabetes by increased endothelial tetrahydrobiopterin synthesis in targeted GTP cyclohydrolase transgenic mice
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Tetrahydrobiopterin-dependent preservation of nitric oxide-mediated endothelial function in diabetes by targeted transgenic GTP-cyclohydrolase I over-expression
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Endothelial-targeted GTP cyclohydrolase I overexpression increases endothelial tetrahydrobiopterin levels and preserves eNOS coupling in eNOS overexpressing mice
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Increased endothelial tetrahydrobiopterin synthesis by targeted transgenic GTP-cyclohydrolase I overexpression reduces endothelial dysfunction and atherosclerosis in ApoE-knockout mice.
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Endotoxemia-related acute kidney injury in transgenic mice with endothelial overexpression of GTP cyclohydrolase-1.
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Nitric oxide bioactivity in ApoE -/- mice is maintained by increased endothelial tetrahydrobiopterin synthesis via targeted GTP cyclohydrolase-1 over-expression
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Stoichiometric relationships between endothelial tetrahydrobiopterin, endothelial NO synthase (eNOS) activity, and eNOS coupling in vivo: insights from transgenic mice with endothelial-targeted GTP cyclohydrolase 1 and eNOS overexpression.
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Cell-autonomous role of endothelial GTP cyclohydrolase 1 and tetrahydrobiopterin in blood pressure regulation.
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Cell-autonomous role of endothelial GTP cyclohydrolase 1 and tetrahydrobiopterin in blood pressure regulation
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GTP cyclohydrolase I expression, protein, and activity determine intracellular tetrahydrobiopterin levels, independent of GTP cyclohydrolase feedback regulatory protein expression.
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Endothelial-targeted GTP cyclohydrolase I overexpression prevents blood pressure progression in mineralocorticoid hypertension\
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303A cell-Autonomous role for endothelial GTP cyclohydrolase 1 and tetrahydrobiopterin in blood pressure regulation.
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GTP cyclohydrolase I gene transfer augments intracellular tetrahydrobiopterin in human endothelial cells: effects on nitric oxide synthase activity, protein levels and dimerisation.
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Endothelial GTP cyclohydrolase and tetrahydrobiopterin regulate gestational blood pressure, uteroplacental remodeling and fetal growth
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Regulation of endothelial nitric oxide synthase (eNOS) by tetrahydrobiopterin in vascular disease
ανά: Alp, N, κ.ά.
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Endothelial nitric oxide synthase dysfunction in diabetic mice: importance of tetrahydrobiopterin in eNOS dimerisation.
ανά: Cai, S, κ.ά.
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Relationships between nitric oxide-mediated endothelial function, eNOS coupling and blood pressure revealed by eNOS-GTP cyclohydrolase 1 double transgenic mice.
ανά: Adlam, D, κ.ά.
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Endothelium-targeted transgenic GTP-cyclohydrolase I overexpression inhibits neointima formation in mouse carotid artery.
ανά: Liao, S, κ.ά.
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PRESERVATION OF ENDOTHELIAL GTP CYCLOHYDROLASE I ACTIVITY AND IMPROVEMENT OF RENAL NITRIC OXIDE AVAILABILITY PREVENT THE DEVELOPMENT OF DIABETIC NEPHROPATHY
ανά: Satoh, M, κ.ά.
Έκδοση: (2012)

Reduced levels of tetrahydrobiopterin in diabetic mouse model: Effects on endothelial function and nitric oxide (NO) synthase dimerisation
ανά: Cai, S, κ.ά.
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Adenovirus-mediated GTP cyclohydrolase I gene delivery augments tetrahydrobiopterin and restores nitric oxide synthase function in hyperglycaemic human aortic endothelial cells
ανά: Cai, S, κ.ά.
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Adenovirus-mediated GTP cyclohydrolase I gene delivery augments tetrahydrobiopterin and restores nitric oxide synthase function in hyperglycaemic human aortic endothelial cells
ανά: Cai, S, κ.ά.
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Increased endothelial tetrahydrobiopterin levels in GTPCH-transgenic mice
ανά: Alp, N, κ.ά.
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Regulation of endothelial nitric oxide synthase by tetrahydrobiopterin in vascular disease.
ανά: Alp, N, κ.ά.
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Cardiomyocyte-Targeted Overexpression of GTP Cyclohydrolase-1 Increases Myocyte Lusitropy and Reduces Superoxide Production
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GTP cyclohydrolase I gene transfer reverses tetrahydrobiopterin deficiency and increases nitric oxide synthesis in endothelial cells and isolated vessels from diabetic rats.
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Systemic adenovirus-mediated gene transfer of human GTP cyclohydrolase-1 increases liver, plasma and aortic tetrahydrobiopterin levels in mice
ανά: Alp, N, κ.ά.
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Cardiomyocyte GTP cyclohydrolase 1 and tetrahydrobiopterin increase NOS1 activity and accelerate myocardial relaxation
ανά: Carnicer, R, κ.ά.
Έκδοση: (2012)

Cardiomyocyte GTP cyclohydrolase 1 and tetrahydrobiopterin increase NOS1 activity and accelerate myocardial relaxation
ανά: Carnicer, R, κ.ά.
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Endothelium-targeted GTP cyclohydrolase I overexpression inhibits wire injury-induced restenosis in mouse carotid artery
ανά: Chen, A, κ.ά.
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Cardiomyocyte-targeted overexpression of GTP cyclohydrolase-1 increases nNOS activity and hastens myocardial relaxation
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Endothelium-specific GTP cyclohydrolase I overexpression attenuates blood pressure progression in salt-sensitive low-renin hypertension.
ανά: Du, Y, κ.ά.
Έκδοση: (2008)

Increased endothelial tetrahydrobiopterin levels by GTPCH over expression in transgenic mice prevents diabetic endothelial dysfunction
ανά: Alp, N, κ.ά.
Έκδοση: (2003)

Increased GTP-cyclohydrolase I expression but not vitamin C treatment restored accelerated atherosclerotic lesion formation in apolipoprotein E-deficient mice overexpressing endothelial nitric oxide synthase
ανά: Takaya, T, κ.ά.
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Quantitative regulation of intracellular endothelial nitric-oxide synthase (eNOS) coupling by both tetrahydrobiopterin-eNOS stoichiometry and biopterin redox status: insights from cells with tet-regulated GTP cyclohydrolase I expression.
ανά: Crabtree, M, κ.ά.
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Endothelial tetrahydrobiopterin deficiency accelerates atherosclerotic progression by nitric oxide synthase uncoupling
ανά: Khoo, J, κ.ά.
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GTP cyclohydrolase I deficiency results in oxidative stress and pulmonary hypertension
ανά: Khoo, J, κ.ά.
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