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Effect of transglutaminase 2 (TG2) deficiency on atherosclerotic plaque stability in the apolipoprotein E deficient mouse.

Williams H, Pease RJ, Newell LM, Cordell PA, Graham RM, Kearney MT, Jackson CL, Grant PJ - Atherosclerosis (2009)

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.

View Article: PubMed Central - PubMed

Affiliation: Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.

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Mouse proximal brachiocephalic artery plaques. Scale bar represents 25 μm in Panels B, D, F and H. Panel (A): TG2 wild-type mouse stained for TG2. TG2 antigen is present on the apparently normal endothelium and on various cells within the shoulder region and in the necrotic core, but is not present on the cap surface. Panel (B): Higher power detail of view of part of Panel A. Panel (C): Negative control, TG2 wild-type mouse processed without the primary antibody. Panel (D): Higher power detail of view of part of Panel C. Panel (E): TG2 knockout mouse stained for TG2 antigen. Panel (F): Higher power detail of view of part of Panel E. Panel (G): TG2 wild-type mouse stained for α-smooth muscle actin. Panel (H): Higher power detail of view of part of Panel G.
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fig1: Mouse proximal brachiocephalic artery plaques. Scale bar represents 25 μm in Panels B, D, F and H. Panel (A): TG2 wild-type mouse stained for TG2. TG2 antigen is present on the apparently normal endothelium and on various cells within the shoulder region and in the necrotic core, but is not present on the cap surface. Panel (B): Higher power detail of view of part of Panel A. Panel (C): Negative control, TG2 wild-type mouse processed without the primary antibody. Panel (D): Higher power detail of view of part of Panel C. Panel (E): TG2 knockout mouse stained for TG2 antigen. Panel (F): Higher power detail of view of part of Panel E. Panel (G): TG2 wild-type mouse stained for α-smooth muscle actin. Panel (H): Higher power detail of view of part of Panel G.

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).


Effect of transglutaminase 2 (TG2) deficiency on atherosclerotic plaque stability in the apolipoprotein E deficient mouse.

Williams H, Pease RJ, Newell LM, Cordell PA, Graham RM, Kearney MT, Jackson CL, Grant PJ - Atherosclerosis (2009)

Mouse proximal brachiocephalic artery plaques. Scale bar represents 25 μm in Panels B, D, F and H. Panel (A): TG2 wild-type mouse stained for TG2. TG2 antigen is present on the apparently normal endothelium and on various cells within the shoulder region and in the necrotic core, but is not present on the cap surface. Panel (B): Higher power detail of view of part of Panel A. Panel (C): Negative control, TG2 wild-type mouse processed without the primary antibody. Panel (D): Higher power detail of view of part of Panel C. Panel (E): TG2 knockout mouse stained for TG2 antigen. Panel (F): Higher power detail of view of part of Panel E. Panel (G): TG2 wild-type mouse stained for α-smooth muscle actin. Panel (H): Higher power detail of view of part of Panel G.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC2874840&req=5

fig1: Mouse proximal brachiocephalic artery plaques. Scale bar represents 25 μm in Panels B, D, F and H. Panel (A): TG2 wild-type mouse stained for TG2. TG2 antigen is present on the apparently normal endothelium and on various cells within the shoulder region and in the necrotic core, but is not present on the cap surface. Panel (B): Higher power detail of view of part of Panel A. Panel (C): Negative control, TG2 wild-type mouse processed without the primary antibody. Panel (D): Higher power detail of view of part of Panel C. Panel (E): TG2 knockout mouse stained for TG2 antigen. Panel (F): Higher power detail of view of part of Panel E. Panel (G): TG2 wild-type mouse stained for α-smooth muscle actin. Panel (H): Higher power detail of view of part of Panel G.
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).

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.

View Article: PubMed Central - PubMed

Affiliation: Bristol Heart Institute, University of Bristol, Level 7, Bristol Royal Infirmary, Bristol BS2 8HW, UK.

Show MeSH
Related in: MedlinePlus