Increased O -GlcNAcylation of Endothelial Nitric Oxide Synthase Compromises the Anti-contractile Properties of Perivascular Adipose Tissue in Metabolic Syndrome
Under physiological conditions, the perivascular adipose tissue (PVAT) negatively modulates vascular contractility. This property is lost in experimental and human obesity and in the metabolic syndrome, indicating that changes in PVAT function may contribute to vascular dysfunction associated with i...
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Published in | Frontiers in physiology Vol. 9; p. 341 |
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Main Authors | , , , , , , , |
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Abstract | Under physiological conditions, the perivascular adipose tissue (PVAT) negatively modulates vascular contractility. This property is lost in experimental and human obesity and in the metabolic syndrome, indicating that changes in PVAT function may contribute to vascular dysfunction associated with increased body weight and hyperglycemia. The
-linked β-N-acetylglucosamine (
-GlcNAc) modification of proteins (
-GlcNAcylation) is a unique posttranslational process that integrates glucose metabolism with intracellular protein activity. Increased flux of glucose through the hexosamine biosynthetic pathway and the consequent increase in tissue-specific
-GlcNAc modification of proteins have been linked to multiple facets of vascular dysfunction in diabetes and other pathological conditions. We hypothesized that chronic consumption of glucose, a condition that progresses to metabolic syndrome, leads to increased
-GlcNAc modification of proteins in the PVAT, decreasing its anti-contractile effects. Therefore, the current study was devised to determine whether a high-sugar diet increases
-GlcNAcylation in the PVAT and how increased
-GlcNAc interferes with PVAT vasorelaxant function. To assess molecular mechanisms by which
-GlcNAc contributes to PVAT dysfunction, thoracic aortas surrounded by PVAT were isolated from Wistar rats fed either a control or high sugar diet, for 10 and 12 weeks. Rats chronically fed a high sugar diet exhibited metabolic syndrome features, increased
-GlcNAcylated-proteins in the PVAT and loss of PVAT anti-contractile effect. PVAT from high sugar diet-fed rats for 12 weeks exhibited decreased NO formation, reduced expression of endothelial nitric oxide synthase (eNOS) and increased
-GlcNAcylation of eNOS. High sugar diet also decreased OGA activity and increased superoxide anion generation in the PVAT. Visceral adipose tissue samples from hyperglycemic patients showed increased levels of
-GlcNAc-modified proteins, increased ROS generation and decreased OGA activity. These data indicate that
-GlcNAcylation contributes to metabolic syndrome-induced PVAT dysfunction and that
-GlcNAcylation of eNOS may be targeted in the development of novel therapies for vascular dysfunction in conditions associated with hyperglycemia. |
---|---|
AbstractList | Under physiological conditions, the perivascular adipose tissue (PVAT) negatively modulates vascular contractility. This property is lost in experimental and human obesity and in the metabolic syndrome, indicating that changes in PVAT function may contribute to vascular dysfunction associated with increased body weight and hyperglycemia. The
O
-linked β-N-acetylglucosamine (
O
-GlcNAc) modification of proteins (
O
-GlcNAcylation) is a unique posttranslational process that integrates glucose metabolism with intracellular protein activity. Increased flux of glucose through the hexosamine biosynthetic pathway and the consequent increase in tissue-specific
O
-GlcNAc modification of proteins have been linked to multiple facets of vascular dysfunction in diabetes and other pathological conditions. We hypothesized that chronic consumption of glucose, a condition that progresses to metabolic syndrome, leads to increased
O
-GlcNAc modification of proteins in the PVAT, decreasing its anti-contractile effects. Therefore, the current study was devised to determine whether a high-sugar diet increases
O
-GlcNAcylation in the PVAT and how increased
O
-GlcNAc interferes with PVAT vasorelaxant function. To assess molecular mechanisms by which
O
-GlcNAc contributes to PVAT dysfunction, thoracic aortas surrounded by PVAT were isolated from Wistar rats fed either a control or high sugar diet, for 10 and 12 weeks. Rats chronically fed a high sugar diet exhibited metabolic syndrome features, increased
O
-GlcNAcylated-proteins in the PVAT and loss of PVAT anti-contractile effect. PVAT from high sugar diet-fed rats for 12 weeks exhibited decreased NO formation, reduced expression of endothelial nitric oxide synthase (eNOS) and increased
O
-GlcNAcylation of eNOS. High sugar diet also decreased OGA activity and increased superoxide anion generation in the PVAT. Visceral adipose tissue samples from hyperglycemic patients showed increased levels of
O
-GlcNAc-modified proteins, increased ROS generation and decreased OGA activity. These data indicate that
O
-GlcNAcylation contributes to metabolic syndrome-induced PVAT dysfunction and that
O
-GlcNAcylation of eNOS may be targeted in the development of novel therapies for vascular dysfunction in conditions associated with hyperglycemia. Under physiological conditions, the perivascular adipose tissue (PVAT) negatively modulates vascular contractility. This property is lost in experimental and human obesity and in the metabolic syndrome, indicating that changes in PVAT function may contribute to vascular dysfunction associated with increased body weight and hyperglycemia. The -linked β-N-acetylglucosamine ( -GlcNAc) modification of proteins ( -GlcNAcylation) is a unique posttranslational process that integrates glucose metabolism with intracellular protein activity. Increased flux of glucose through the hexosamine biosynthetic pathway and the consequent increase in tissue-specific -GlcNAc modification of proteins have been linked to multiple facets of vascular dysfunction in diabetes and other pathological conditions. We hypothesized that chronic consumption of glucose, a condition that progresses to metabolic syndrome, leads to increased -GlcNAc modification of proteins in the PVAT, decreasing its anti-contractile effects. Therefore, the current study was devised to determine whether a high-sugar diet increases -GlcNAcylation in the PVAT and how increased -GlcNAc interferes with PVAT vasorelaxant function. To assess molecular mechanisms by which -GlcNAc contributes to PVAT dysfunction, thoracic aortas surrounded by PVAT were isolated from Wistar rats fed either a control or high sugar diet, for 10 and 12 weeks. Rats chronically fed a high sugar diet exhibited metabolic syndrome features, increased -GlcNAcylated-proteins in the PVAT and loss of PVAT anti-contractile effect. PVAT from high sugar diet-fed rats for 12 weeks exhibited decreased NO formation, reduced expression of endothelial nitric oxide synthase (eNOS) and increased -GlcNAcylation of eNOS. High sugar diet also decreased OGA activity and increased superoxide anion generation in the PVAT. Visceral adipose tissue samples from hyperglycemic patients showed increased levels of -GlcNAc-modified proteins, increased ROS generation and decreased OGA activity. These data indicate that -GlcNAcylation contributes to metabolic syndrome-induced PVAT dysfunction and that -GlcNAcylation of eNOS may be targeted in the development of novel therapies for vascular dysfunction in conditions associated with hyperglycemia. Under physiological conditions, the perivascular adipose tissue (PVAT) negatively modulates vascular contractility. This property is lost in experimental and human obesity and in the metabolic syndrome, indicating that changes in PVAT function may contribute to vascular dysfunction associated with increased body weight and hyperglycemia. The O-linked β-N-acetylglucosamine (O-GlcNAc) modification of proteins (O-GlcNAcylation) is a unique posttranslational process that integrates glucose metabolism with intracellular protein activity. Increased flux of glucose through the hexosamine biosynthetic pathway and the consequent increase in tissue-specific O-GlcNAc modification of proteins have been linked to multiple facets of vascular dysfunction in diabetes and other pathological conditions. We hypothesized that chronic consumption of glucose, a condition that progresses to metabolic syndrome, leads to increased O-GlcNAc modification of proteins in the PVAT, decreasing its anti-contractile effects. Therefore, the current study was devised to determine whether a high-sugar diet increases O-GlcNAcylation in the PVAT and how increased O-GlcNAc interferes with PVAT vasorelaxant function. To assess molecular mechanisms by which O-GlcNAc contributes to PVAT dysfunction, thoracic aortas surrounded by PVAT were isolated from Wistar rats fed either a control or high sugar diet, for 10 and 12 weeks. Rats chronically fed a high sugar diet exhibited metabolic syndrome features, increased O-GlcNAcylated-proteins in the PVAT and loss of PVAT anti-contractile effect. PVAT from high sugar diet-fed rats for 12 weeks exhibited decreased NO formation, reduced expression of endothelial nitric oxide synthase (eNOS) and increased O-GlcNAcylation of eNOS. High sugar diet also decreased OGA activity and increased superoxide anion generation in the PVAT. Visceral adipose tissue samples from hyperglycemic patients showed increased levels of O-GlcNAc-modified proteins, increased ROS generation and decreased OGA activity. These data indicate that O-GlcNAcylation contributes to metabolic syndrome-induced PVAT dysfunction and that O-GlcNAcylation of eNOS may be targeted in the development of novel therapies for vascular dysfunction in conditions associated with hyperglycemia. |
Author | Garcia, Luis V Rassi, Diane M Tostes, Rita C Alves, Juliano V da Silva, Josiane F Lobato, Núbia de Souza da Costa, Rafael M Dias, Thiago B |
AuthorAffiliation | 1 Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo , Ribeirao Preto , Brazil 3 Department of Physiology, Institute of Health Sciences, Federal University of Goias , Jatai , Brazil 2 Department of Biomechanics, Medicine and Locomotive Apparatus Rehabilitation, Ribeirao Preto Medical School, University of Sao Paulo , Ribeirao Preto , Brazil |
AuthorAffiliation_xml | – name: 3 Department of Physiology, Institute of Health Sciences, Federal University of Goias , Jatai , Brazil – name: 2 Department of Biomechanics, Medicine and Locomotive Apparatus Rehabilitation, Ribeirao Preto Medical School, University of Sao Paulo , Ribeirao Preto , Brazil – name: 1 Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo , Ribeirao Preto , Brazil |
Author_xml | – sequence: 1 givenname: Rafael M surname: da Costa fullname: da Costa, Rafael M organization: Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil – sequence: 2 givenname: Josiane F surname: da Silva fullname: da Silva, Josiane F organization: Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil – sequence: 3 givenname: Juliano V surname: Alves fullname: Alves, Juliano V organization: Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil – sequence: 4 givenname: Thiago B surname: Dias fullname: Dias, Thiago B organization: Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil – sequence: 5 givenname: Diane M surname: Rassi fullname: Rassi, Diane M organization: Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil – sequence: 6 givenname: Luis V surname: Garcia fullname: Garcia, Luis V organization: Department of Biomechanics, Medicine and Locomotive Apparatus Rehabilitation, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil – sequence: 7 givenname: Núbia de Souza surname: Lobato fullname: Lobato, Núbia de Souza organization: Department of Physiology, Institute of Health Sciences, Federal University of Goias, Jatai, Brazil – sequence: 8 givenname: Rita C surname: Tostes fullname: Tostes, Rita C organization: Department of Pharmacology, Ribeirao Preto Medical School, University of Sao Paulo, Ribeirao Preto, Brazil |
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ContentType | Journal Article |
Copyright | Copyright © 2018 da Costa, Silva, Alves, Dias, Rassi, Garcia, Lobato and Tostes. 2018 da Costa, Silva, Alves, Dias, Rassi, Garcia, Lobato and Tostes |
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Keywords | vascular function eNOS PVAT high-sugar diet O-GlcNAc |
Language | English |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Reviewed by: Brett M. Mitchell, Texas A&M Health Science Center, United States; Rudolf Schubert, Universität Heidelberg, Germany This article was submitted to Vascular Physiology, a section of the journal Frontiers in Physiology Edited by: Stephanie W. Watts, Michigan State University, United States |
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Title | Increased O -GlcNAcylation of Endothelial Nitric Oxide Synthase Compromises the Anti-contractile Properties of Perivascular Adipose Tissue in Metabolic Syndrome |
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