Transglutaminase 2 deficiency decreases plaque fibrosis and increases plaque inflammation in apolipoprotein-E-deficient mice

J Vasc Res. 2010;47(3):231-40. doi: 10.1159/000255966. Epub 2009 Nov 6.

Abstract

Aim: Transglutaminase 2 (TG2) is important for the deposition and stability of the extracellular matrix via effects on cross-linking of matrix proteins and transforming growth factor beta (TGFbeta) activity. The purpose of this study was to investigate the effect of TG2 deficiency on the composi- tion of atherosclerotic plaques.

Methods: Apolipoprotein E (ApoE)(-/-) mice were crossbred with TG2(-/-) mice to obtain ApoE(-/-)TG2(-/-) mice. ApoE(-/-) and ApoE(-/-)TG2(-/-) mice were fed a Western-type diet for 16 or 30 weeks to determine the effect of TG2 deficiency on early and advanced atherosclerosis, respectively.

Results: Atherosclerotic plaques of ApoE(-/-)TG2(-/-) mice showed decreased cross-linking of matrix proteins, as well as decreased nuclear staining for phospho-Smad2/-Smad3, indicative of decreased TGFbeta activity. Compared to ApoE(-/-) mice, plaque area was decreased by 45 and 48% in ApoE(-/-)TG2(-/-) mice after 16 and 30 weeks, respectively. Sirius red staining showed a significant decrease in collagen content in early and advanced atherosclerotic plaques of ApoE(-/-)TG2(-/-) mice. Furthermore, there was a significant increase in macrophages in advanced atherosclerotic plaques of ApoE(-/-)TG2(-/-) mice.

Conclusion: TG2 deficiency resulted in a decreased collagen content and increased inflammation, which are features of a more unstable plaque.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apolipoproteins E / deficiency*
  • Apolipoproteins E / genetics
  • Atherosclerosis / enzymology*
  • Atherosclerosis / genetics
  • Atherosclerosis / pathology
  • Atherosclerosis / prevention & control
  • Collagen / metabolism
  • Disease Models, Animal
  • Disease Progression
  • Extracellular Matrix Proteins / metabolism
  • Female
  • Fibrosis
  • GTP-Binding Proteins / deficiency*
  • GTP-Binding Proteins / genetics
  • Inflammation / enzymology*
  • Inflammation / genetics
  • Inflammation / pathology
  • Macrophages / pathology
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Protein Glutamine gamma Glutamyltransferase 2
  • Rupture
  • Time Factors
  • Transforming Growth Factor beta / metabolism
  • Transglutaminases / deficiency*
  • Transglutaminases / genetics

Substances

  • Apolipoproteins E
  • Extracellular Matrix Proteins
  • Transforming Growth Factor beta
  • Collagen
  • Protein Glutamine gamma Glutamyltransferase 2
  • Transglutaminases
  • GTP-Binding Proteins