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Tumor necrosis factor-alpha does not mediate diabetes-induced vascular inflammation in mice.

Öhman, Jenny LU ; Nordin Fredrikson, Gunilla LU ; Berglund, Lisa LU ; Gustavsson, Carin LU ; Bengtsson, Eva LU ; Smith, Maj-Lis LU ; Agardh, Carl-David LU ; Agardh, Elisabet LU ; Jovinge, Stefan LU and Gomez, Maria LU , et al. (2009) In Arteriosclerosis, Thrombosis and Vascular Biology 29(10). p.1465-1470
Abstract
OBJECTIVE: Vascular inflammation is a key feature of both micro- and macrovascular complications in diabetes. Several lines of evidence have implicated the cytokine tumor necrosis factor (TNF) alpha as an important mediator of inflammation in diabetes. In the present study we evaluated the role of TNF alpha in streptozotocin (STZ)-induced diabetes on vascular inflammation in C57BL/6 wild-type and apoE-/- mice. METHODS AND RESULTS: Diabetes increased the expression of vascular cell adhesion molecule (VCAM)-1 in cerebral arteries 150 m in diameter as well as the macrophage accumulation in aortic root atherosclerotic plaques in apoE-/- mice. A more pronounced vascular inflammatory response was observed in diabetic TNF alpha-deficient apoE-/-... (More)
OBJECTIVE: Vascular inflammation is a key feature of both micro- and macrovascular complications in diabetes. Several lines of evidence have implicated the cytokine tumor necrosis factor (TNF) alpha as an important mediator of inflammation in diabetes. In the present study we evaluated the role of TNF alpha in streptozotocin (STZ)-induced diabetes on vascular inflammation in C57BL/6 wild-type and apoE-/- mice. METHODS AND RESULTS: Diabetes increased the expression of vascular cell adhesion molecule (VCAM)-1 in cerebral arteries 150 m in diameter as well as the macrophage accumulation in aortic root atherosclerotic plaques in apoE-/- mice. A more pronounced vascular inflammatory response was observed in diabetic TNF alpha-deficient apoE-/- mice. These mice were also characterized by increased accumulation of IgG and IgM autoantibodies in atherosclerotic lesions. Diabetes also increased VCAM-1 expression and plaque formation in apoE-competent TNF alpha -/- mice, whereas no such effects were observed in C57BL/6 wild-type mice. CONCLUSIONS: The present findings suggest that TNF alpha does not mediate diabetic-induced vascular inflammation in mice and reveal an unexpected protective role for TNF alpha. These effects are partly attributable to a direct antiinflammatory role of TNF alpha, but may also reflect a defective development of the immune system in these mice. (Less)
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keywords
Lipoproteins, Inflammation: etiology, Diabetic Angiopathies: etiology, Experimental: complications, Diabetes Mellitus, Cerebral Arteries: chemistry, Blood Glucose: analysis, Autoantibodies: analysis, Apolipoproteins E: physiology, Atherosclerosis: etiology, Vascular Cell Adhesion Molecule-1: blood, LDL: immunology, Tumor Necrosis Factor-alpha: physiology
in
Arteriosclerosis, Thrombosis and Vascular Biology
volume
29
issue
10
pages
1465 - 1470
publisher
American Heart Association
external identifiers
  • wos:000269848600012
  • pmid:19755528
  • scopus:70349576927
ISSN
1524-4636
DOI
10.1161/ATVBAHA.109.193862
language
English
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yes
id
7b02a78e-536f-4b6c-b655-1f681c9c00ba (old id 1483468)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/19755528?dopt=Abstract
date added to LUP
2009-10-07 09:26:23
date last changed
2017-01-01 07:40:19
@article{7b02a78e-536f-4b6c-b655-1f681c9c00ba,
  abstract     = {OBJECTIVE: Vascular inflammation is a key feature of both micro- and macrovascular complications in diabetes. Several lines of evidence have implicated the cytokine tumor necrosis factor (TNF) alpha as an important mediator of inflammation in diabetes. In the present study we evaluated the role of TNF alpha in streptozotocin (STZ)-induced diabetes on vascular inflammation in C57BL/6 wild-type and apoE-/- mice. METHODS AND RESULTS: Diabetes increased the expression of vascular cell adhesion molecule (VCAM)-1 in cerebral arteries 150 m in diameter as well as the macrophage accumulation in aortic root atherosclerotic plaques in apoE-/- mice. A more pronounced vascular inflammatory response was observed in diabetic TNF alpha-deficient apoE-/- mice. These mice were also characterized by increased accumulation of IgG and IgM autoantibodies in atherosclerotic lesions. Diabetes also increased VCAM-1 expression and plaque formation in apoE-competent TNF alpha -/- mice, whereas no such effects were observed in C57BL/6 wild-type mice. CONCLUSIONS: The present findings suggest that TNF alpha does not mediate diabetic-induced vascular inflammation in mice and reveal an unexpected protective role for TNF alpha. These effects are partly attributable to a direct antiinflammatory role of TNF alpha, but may also reflect a defective development of the immune system in these mice.},
  author       = {Öhman, Jenny and Nordin Fredrikson, Gunilla and Berglund, Lisa and Gustavsson, Carin and Bengtsson, Eva and Smith, Maj-Lis and Agardh, Carl-David and Agardh, Elisabet and Jovinge, Stefan and Gomez, Maria and Nilsson, Jan},
  issn         = {1524-4636},
  keyword      = {Lipoproteins,Inflammation: etiology,Diabetic Angiopathies: etiology,Experimental: complications,Diabetes Mellitus,Cerebral Arteries: chemistry,Blood Glucose: analysis,Autoantibodies: analysis,Apolipoproteins E: physiology,Atherosclerosis: etiology,Vascular Cell Adhesion Molecule-1: blood,LDL: immunology,Tumor Necrosis Factor-alpha: physiology},
  language     = {eng},
  number       = {10},
  pages        = {1465--1470},
  publisher    = {American Heart Association},
  series       = {Arteriosclerosis, Thrombosis and Vascular Biology},
  title        = {Tumor necrosis factor-alpha does not mediate diabetes-induced vascular inflammation in mice.},
  url          = {http://dx.doi.org/10.1161/ATVBAHA.109.193862},
  volume       = {29},
  year         = {2009},
}