کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10738401 | 1046704 | 2011 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Antioxidant signaling via Nrf2 counteracts lipopolysaccharide-mediated inflammatory responses in foam cell macrophages
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کلمات کلیدی
bZIPEMSADMNQKelch-like ECH-associated protein-1Heme oxygenase-1iNOSDPICOX-2HO-1NACFCMLPSC/EBP - C / EBPDMSO - DMSON-acetylcysteine - N-استیل سیستئینinterleukin - اینترلوکینelectrophoretic mobility-shift assay - تحرک انتقال الکتریکی - تحرک تغییرdiphenyliodonium - دیفنیلیدونیمDimethyl sulfoxide - دیمتیل سولفواکسیدbasic-leucine zipper - زیپ پایه لوسینinducible nitric oxide synthase - سنتاز اکسید نیتریک القاییCyclooxygenase-2 - سیکلوکوکسیژناز2antioxidant response element - عنصر پاسخ آنتی اکسیدانKeap-1 - فروش-1Low-density lipoprotein - لیپوپروتئین کم چگالی یا الدیال LDL - لیپوپروتئین کم چگالی(کلسترول بد)lipopolysaccharide - لیپوپلی ساکاریدARE - هستندHydroethidine - هیدروتیدینCCAAT/enhancer binding protein - پروتئین اتصال CCAAT / enhancer
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Inflammatory conditions and oxidative stress contribute to the development of atherosclerosis. Nuclear factor E2-related factor 2 (Nrf2) is a redox-sensitive transcription factor known for its antioxidant, anti-inflammatory, and, thus, cell-protective properties. Its role in effecting a deactivated state of oxidized low-density lipoprotein (oxLDL)-generated foam cell macrophages (FCMs), a prevailing cellular phenotype of atherosclerotic lesions, has not been investigated yet. In this study RAW264.7- or mouse peritoneal macrophage-derived FCMs showed reduced mRNA expression of proinflammatory cytokines such as IL-1β and IL-6 and an attenuated production of reactive oxygen species (ROS), as analyzed by hydroethidine in response to lipopolysaccharide (LPS) and compared to LPS-treated control macrophages. In peritoneal FCMs from Nrf2â/â mice (C57BL/6J), the LPS-induced proinflammatory response was restored. OxLDL induced heme oxygenase (HO)-1, which was Nrf2-dependent, and inhibition of HO-1 activity in FCMs using zinc protoporphyrin-IX allowed the cells to regain a proinflammatory phenotype. Mechanistically, oxLDL attenuated ROS-dependent activation of CCAAT/enhancer binding protein (C/EBP) family members in FCMs, thereby reducing cytokine expression. Thus, in FCMs the Nrf2/HO-1 axis intervenes in LPS signaling. ROS production is impaired, C/EBP transactivation is reduced, and consequently the expression of proinflammatory mediators is attenuated, thereby shaping a desensitized FCM phenotype. This macrophage phenotype may be important for the progression of atherosclerosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Free Radical Biology and Medicine - Volume 50, Issue 10, 15 May 2011, Pages 1382-1391
Journal: Free Radical Biology and Medicine - Volume 50, Issue 10, 15 May 2011, Pages 1382-1391
نویسندگان
Anne-Marie Kuhn, Nico Tzieply, Martina Victoria Schmidt, Andreas von Knethen, Dmitry Namgaladze, Masayuki Yamamoto, Bernhard Brüne,