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Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE-/-mice

  • Sabrina Hsiung
  • Anki Knutsson
  • Jenifer Vallejo
  • Pontus Dunér
  • Suvi E. Heinonen
  • Ann Cathrine Jönsson-Rylander
  • Eva Bengtsson
  • Jan Nilsson
  • Anna Hultgårdh-Nilsson
Publishing year: 2018-12-01
Language: English
Publication/Series: Scientific Reports
Volume: 8
Issue: 1
Document type: Journal article
Publisher: Nature Publishing Group

Abstract english

The mechanisms responsible for macrovascular complications in diabetes remain to be fully understood. Recent studies have identified impaired vascular repair as a possible cause of plaque vulnerability in diabetes. This notion is supported by observations of a reduced content of fibrous proteins and smooth muscle cell mitogens in carotid endarterectomy from diabetic patients along with findings of decreased circulating levels of endothelial progenitor cells. In the present study we used a diabetic mouse model to characterize how hyperglycemia affects arterial repair responses. We induced atherosclerotic plaque formation in ApoE-deficient (ApoE-/-) and heterozygous glucokinase knockout ApoE-deficient mice (ApoE-/-GK+/-) mice with a shear stress-modifying cast. There were no differences in cholesterol or triglyceride levels between the ApoE-/-A nd ApoE-/-GK+/-mice. Hyperglycemia did not affect the size of the formed atherosclerotic plaques, and no effects were seen on activation of cell proliferation, smooth muscle cell content or on the expression and localization of collagen, elastin and several other extracellular matrix proteins. The present study demonstrates that hyperglycemia per se has no significant effects on tissue repair processes in injured mouse carotid arteries, suggesting that other mechanisms are involved in diabetic plaque vulnerability.


  • Cardiac and Cardiovascular Systems


  • Vessel Wall Biology
  • Cardiovascular Research - Immunity and Athersosclerosis
  • Cardiovascular Research - Matrix and Inflammation in Atherosclerosis
  • ISSN: 2045-2322
E-mail: jan [dot] nilsson [at] med [dot] lu [dot] se

Lund University Diabetes Centre, CRC, SUS Malmö, Jan Waldenströms gata 35, House 91:12. SE-214 28 Malmö. Telephone: +46 40 39 10 00