کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10770837 | 1050836 | 2005 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Loss of lysophospholipase 3 increases atherosclerosis in apolipoprotein E-deficient mice
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کلمات کلیدی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Human LCAT-like lysophospholipase (LLPL), or lysophospholipase 3, was first identified in vitro, in foam cells derived from THP-1 cells. We demonstrated that LLPL was present in foam cells in the severe atherosclerotic lesions that develop in apolipoprotein E-null (apoEâ/â) mice. This indicated that LLPL might affect lipid metabolisms in foam cells and, therefore, atherogenesis. Accordingly, we created LLPL-knockout mice by gene targeting and crossed them with apoEâ/â mice. We showed that the absence of LLPL increased lesion formation markedly in apoEâ/â mice but had little effect on the plasma-lipid profile. In addition, LLPL-deficient peritoneal macrophages were more sensitive to apoptosis induced by exposure to oxidized low-density lipoprotein. LLPL might provide a link between apoptosis in macrophages and atherogenesis. Our data demonstrate that LLPL activity is anti-atherogenic and indicate that the regulation of this enzyme might be a novel drug target for the treatment of atherosclerosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 330, Issue 1, 29 April 2005, Pages 104-110
Journal: Biochemical and Biophysical Research Communications - Volume 330, Issue 1, 29 April 2005, Pages 104-110
نویسندگان
Yoshio Taniyama, Hiromitsu Fuse, Tomoko Satomi, Ryuichi Tozawa, Yoshitaka Yasuhara, Kozo Shimakawa, Sachio Shibata, Masahiko Hattori, Mitsugu Nakata, Shigehisa Taketomi,