Effect of transglutaminase 2 (TG2) deficiency on atherosclerotic plaque stability in the apolipoprotein E deficient mouse.
Bottom Line: Transglutaminase 2 (TG2), a cross-linking enzyme that confers supra-molecular structures with extra rigidity and resistance against proteolytic degradation, is expressed in the shoulder regions of human atherosclerotic plaques.It has been proposed that TG2 prevents tearing and promotes plaque repair at these potential weak points, and also promotes ectopic calcification of arteries.The frequency of buried fibrous caps within brachiocephalic plaques was significantly higher in male than in female mice, but TG2 deficiency had no effect on either gender.
Affiliation: Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.Show MeSH
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Mentions: The commercial TG2 anti-serum detected a single band in total mouse liver proteins that co-migrated with guinea pig liver TG2 (not shown). The specificity of immunohistochemical staining of the TG2 anti-serum was confirmed by showing that staining was minimal in spleen from TG2 knockout mice but abundant in spleen from wild-type mice, and that the antibody strongly stained capillary endothelial cells in intestinal villi (Supplementary Fig. 1). In agreement with previous reports, the antibody intensely stained formations of cells in the shoulder regions of human carotid atherosclerotic plaques including the intima of capillaries within the arterial wall (Supplementary Fig. 2). The TG2 antibody strongly stained intact endothelium in brachiocephalic arteries from apoE deficient mice TG2 but also detected small clusters of cells within the shoulder regions of mouse plaques and within the core of the plaque (Fig. 1).
Affiliation: Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.