Nutritional B vitamin deficiency alters the expression of key proteins associated with vascular smooth muscle cell proliferation and migration in the aorta of atherosclerotic apolipoprotein E null mice

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• 作者：Susan J. Duthie (1) (2)
  John H. Beattie (2)
  Margaret-J. Gordon (2)
  Lynn P. Pirie (2)
  Fergus Nicol (2)
  Martin D. Reid (2)
  Gary J. Duncan (2)
  Louise Cantlay (2)
  Graham Horgan (3)
  Christopher J. McNeil (2)
  
• 关键词：Aorta proteome ; ApoE null mice ; Atherosclerosis ; B vitamins ; Hyperhomocysteinemia
• 刊名：Genes & Nutrition
• 出版年：2015
• 出版时间：January 2015
• 年：2015
• 卷：10
• 期：1
• 全文大小：637 KB
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• 作者单位：Susan J. Duthie (1) (2)
  John H. Beattie (2)
  Margaret-J. Gordon (2)
  Lynn P. Pirie (2)
  Fergus Nicol (2)
  Martin D. Reid (2)
  Gary J. Duncan (2)
  Louise Cantlay (2)
  Graham Horgan (3)
  Christopher J. McNeil (2)
  
  1. School of Pharmacy and Life Sciences, Robert Gordon University, Aberdeen, UK
  2. Division of Lifelong Health, Rowett Institute of Nutrition and Health, University of Aberdeen, Aberdeen, UK
  3. Biomathematics and Statistics Scotland (BioSS), Aberdeen, AB21 9SB, UK
  
• ISSN：1865-3499

文摘

Low B vitamin status is linked with human vascular disease. We employed a proteomic and biochemical approach to determine whether nutritional folate deficiency and/or hyperhomocysteinemia altered metabolic processes linked with atherosclerosis in ApoE null mice. Animals were fed either a control fat (C; 4?% w/w lard) or a high-fat [HF; 21?% w/w lard and cholesterol (0/15?% w/w)] diet with different B vitamin compositions for 16?weeks. Aorta tissue was prepared and global protein expression, B vitamin, homocysteine and lipoprotein status measured. Changes in the expression of aorta proteins were detected in response to multiple B vitamin deficiency combined with a high-fat diet (P?P?ApoE null mice. Deregulated expression of these proteins is associated with human atherosclerosis. Cellular pathways altered by B vitamin status included cytoskeletal organisation, cell differentiation and migration, oxidative stress and chronic inflammation. These findings provide new insight into the molecular mechanisms through which B vitamin deficiency may accelerate atherosclerosis.