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Flow patterns regulate hyperglycemia-induced subendothelial matrix remodeling during early atherogenesis.

Jonette Green1, Arif Yurdagul2, Marshall C McInnis1

  • 1Department of Pathology, LSU Health Sciences Center - Shreveport, Biomedical Research Institute, Rm. 6-21, 1501 Kings Hwy, Shreveport, LA 71130, USA.

Atherosclerosis
|January 29, 2014
PubMed
Summary

Diabetic hyperglycemia and disturbed blood flow promote fibronectin deposition in the arterial wall, contributing to early atherosclerosis. This matrix remodeling is regulated by the interplay between glucose levels and blood flow patterns.

Keywords:
AtherosclerosisEndothelialFibronectinHyperglycemiaShear stress

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Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Atherosclerosis Research

Background:

  • Altered subendothelial matrix composition contributes to endothelial dysfunction and early atherosclerotic plaque formation.
  • Hyperglycemia is known to promote endothelial matrix remodeling, but its role in diabetic atherogenesis is not well understood.
  • Early atherosclerotic lesions preferentially form at sites with disturbed blood flow.

Purpose of the Study:

  • To characterize alterations in subendothelial matrix composition during diabetic atherogenesis.
  • To investigate the combined effects of hyperglycemia and blood flow patterns on matrix remodeling.
  • To utilize both in vitro and in vivo model systems for comprehensive analysis.

Main Methods:

  • Streptozotocin-induced diabetes in atherosclerosis-prone ApoE knockout mice.
  • Quantitative reverse transcription polymerase chain reaction (qRT-PCR) array and immunohistochemistry to assess matrix protein expression and deposition.
  • Endothelial cell culture models exposed to varying glucose concentrations and simulated blood flow conditions (laminar vs. disturbed).

Main Results:

  • Diabetic mice exhibited increased expression and deposition of transitional matrix proteins, including fibronectin and thrombospondin-1, in the aortic arch intima.
  • Hyperglycemia-induced matrix deposition was localized to regions of disturbed blood flow, while laminar flow regions were protected.
  • In vitro, laminar flow significantly reduced high glucose-induced fibronectin expression and fibrillogenesis, whereas disturbed flow and static conditions showed similar fibronectin deposition.

Conclusions:

  • Blood flow patterns and hyperglycemia act coordinately to regulate subendothelial fibronectin deposition during the early stages of atherogenesis.
  • These findings highlight a specific mechanism by which diabetes exacerbates atherosclerosis, particularly at sites prone to disturbed blood flow.