Cyclooxygenase 2, toll-like receptor 4 and interleukin 1β mRNA expression in atherosclerotic plaques of type 2 diabetic patients

Inflamm Res. 2014 Oct;63(10):851-8. doi: 10.1007/s00011-014-0759-8. Epub 2014 Aug 6.

Abstract

Objectives and design: Inflammation has a prominent role in the development of atherosclerosis. Type 2 diabetes could contribute to atherosclerosis development by promoting inflammation. This status might accelerate changes in intrinsic vascular wall cells and favor plaque formation. Cyclooxygenase 2 (COX-2) is highly expressed in atherosclerotic plaques. COX-2 gene expression is promoted through activation of toll-like receptor 4 (TLR4) and pro-inflammatory cytokine interleukin 1β (IL1-β). Aim of this study is to investigate whether expression profiles of pro-inflammatory genes such as COX-2, TLR4 and IL1-β in atherosclerotic plaques are altered in type 2 diabetes (T2D).

Methods: Total RNA was isolated from plaques of atherosclerotic patients and expression of COX-2, TLR4, IL1-β analyzed using real-time PCR. Histological analysis was performed on sections of the plaque to establish the degree of instability.

Results: Statistically significant differences in mRNA expression of COX-2 and IL1-β were found in plaques of T2D compared with non-T2D patients. A multi-variable linear regression model suggests that COX-2 mRNA expression is affected by T2D pathology and IL1-β mRNA expression in atherosclerotic plaques.

Conclusions: Our results support the hypothesis that T2D pathology contributes in vivo to increase the inflammatory process associated with the atherosclerotic plaque formation, as shown by an increment of COX-2 and IL1-β mRNA expression.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Cyclooxygenase 2 / genetics*
  • Diabetes Mellitus, Type 2 / genetics*
  • Female
  • Gene Expression
  • Humans
  • Interleukin-1beta / genetics*
  • Male
  • Middle Aged
  • Plaque, Atherosclerotic / genetics*
  • RNA, Messenger / metabolism
  • Toll-Like Receptor 4 / genetics*

Substances

  • Interleukin-1beta
  • RNA, Messenger
  • TLR4 protein, human
  • Toll-Like Receptor 4
  • Cyclooxygenase 2
  • PTGS2 protein, human