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TG2 on the surface of macrophages also facilitates apoptotic cell engulfment [5]?and?[6]. Intracellular TG2 activity is suppressed within healthy cells, but becomes activated following injury and cross-links cellular components to minimize pro-inflammatory leakage [4]. TG2 may therefore play multiple roles in the body's response to tissue damage, and it is induced in human atherosclerotic plaques where it may stabilize against rupture [7]?and?[8]. Recently it has been suggested that TG2 enables smooth muscle cells to transform into chondrocyte-like cells [9], thus promoting ectopic calcification of atherosclerotic arteries and exerting deleterious as well as beneficial effects on lesion development [10]. Apolipoprotein E (apoE) deficient mice, maintained on a high-fat diet, develop INSRR advanced and complex plaques in the proximal brachiocephalic artery [11], [12]?and?[13], although such plaques are rare at other anatomical sites [14]. It has been proposed that these plaques undergo cycles of rupture and repair [14]. The use of mice doubly deficient for apoE and for individual proteinases has identified some that promote lesion development, while indicating others that may be protective [15]?and?[16]. We are using an analogous approach to define the roles of the transglutaminases, examining, in the first instance, TG2. TG2 is a widely expressed and abundant protein, and unlike most other abundant transglutaminases, which have very restricted tissue distributions and functions, TG2 has been implicated in arterial repair. Mice with a targeted disruption of the TG2 gene develop normally for the first year of life [17]?and?[18] BMS-754807 cost but subsequently develop mild abnormalities including glucose intolerance [19]. In the BLZ945 supplier present study, apoE/TG2 double-knockout mice were bred and were compared (at less than 12 months of age), with matched apoE single knockout controls to determine the role of TG2 in plaque rupture and repair and in arterial calcification. The maintenance of the animals, and the procedures used in these studies, were performed in accordance with the guidelines and regulations of the University of Bristol and the United Kingdom Home Office. ApoE [20] and TG2 [17] single knockout mice, both on a mixed C57BL/6, 129 strain background, were crossed and the doubly heterozygous F1 mice were interbred. Tail-tip DNA from the F2 mice and subsequent litters was genotyped by PCR. In the F2 generation, only 1 double homozygote was obtained among 98 mice (p?