Transglutaminase 2 Deficiency Decreases Plaque Fibrosis and Increases Plaque Inflammation in Apolipoprotein-E-Deficient Mice
نویسندگان
چکیده
منابع مشابه
Transglutaminase 2 deficiency decreases plaque fibrosis and increases plaque inflammation in apolipoprotein-E-deficient mice.
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...
متن کاملInterleukin-17A deficiency accelerates unstable atherosclerotic plaque formation in apolipoprotein E-deficient mice.
OBJECTIVE Interleukin(IL)-17A, an inflammatory cytokine, has been implicated in atherosclerosis, in which inflammatory cells within atherosclerotic plaques express IL-17A. However, its role in the development of atheroscelrosis remains to be controversial. METHODS AND RESULTS To directly examine the role of IL-17A in atherosclerosis, we generated apolipoprotein E (ApoE)/IL-17A double-deficien...
متن کاملAtherosclerotic Plaque rupture in Apolipoprotein e−/− Mice
A therosclerotic plaque rupture and subsequent thrombus formation in the culprit lesion are recognized to be the seminal events in the majority of cases of acute coronary syndrome. Plaque stability is determined by many factors, including lipid deposits, oxidative stress, inflammation, and extracellular matrix degradation. Accumulation of lipid in the atherosclerotic lesion increases mechanical...
متن کاملOverexpression of IL-18 decreases intimal collagen content and promotes a vulnerable plaque phenotype in apolipoprotein-E-deficient mice.
OBJECTIVE Although IL-18 has been implicated in atherosclerotic lesion development, little is known about its role in advanced atherosclerotic plaques. This study aims to assess the effect of IL-18 overexpression on the stability of preexisting plaques. METHODS AND RESULTS Atherosclerotic lesions were elicited in carotid arteries of apolipoprotein E (apoE)-deficient mice (n=32) by placement o...
متن کاملPeroxiredoxin 2 deficiency exacerbates atherosclerosis in apolipoprotein E-deficient mice.
RATIONALE Peroxiredoxin 2 (Prdx2), a thiol-specific peroxidase, has been reported to regulate proinflammatory responses, vascular remodeling, and global oxidative stress. OBJECTIVE Although Prdx2 has been proposed to retard atherosclerosis development, no direct evidence and mechanisms have been reported. METHODS AND RESULTS We show that Prdx2 is highly expressed in endothelial and immune c...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
ژورنال
عنوان ژورنال: Journal of Vascular Research
سال: 2010
ISSN: 1423-0135,1018-1172
DOI: 10.1159/000255966