کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2019616 | 1542213 | 2015 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
CYP epoxygenase 2J2 prevents cardiac fibrosis by suppression of transmission of pro-inflammation from cardiomyocytes to macrophages
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کلمات کلیدی
CYP2J2NF-κBα-SMATGF-β1PPARECMEETsalpha smooth muscle actin - آلفا آکتیو عضله صافAngiotensin II - آنژیوتانسین دوepoxyeicosatrienoic acids - اسید اپوکسی اسیاتریتروئینinflammation - التهاب( توروم) ISO - ایزوIsoprenaline - ایسوپرنالینTransforming growth factor-beta 1 - تبدیل فاکتور رشد بتا 1transgene - ترانس ژنEET - خوردنAng II - دومnuclear factor kappa-light-chain-enhancer of activated B cells - فاکتور هسته ای kappa-light-chain-enhancer از سلول های B فعال شده استCardiac fibrosis - فیبروز قلبExtracellular matrix - ماتریکس خارج سلولیheart failure - نارسایی قلبیwild type - نوع وحشی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Cytochrome P450 epoxygenase (CYP450)-derived epoxyeicosatrienoic acids (EETs) are important regulators of cardiac remodeling; but the underlying mechanism remains unclear. The present study aimed to elucidate how EETs regulated cardiac fibrosis in response to isoprenaline (Iso) or angiotensin (Ang) II. Cardiac-specific human CYP2J2 transgenic mice (Tr) and wild-type (WT) C57BL/6 littermates were infused with Iso- or Ang II. Two weeks after infusion, Tr mice showed more alleviative cardiac fibrosis and inflammation compared with WT mice. In vitro, we found Iso or Ang II induced nuclear transfer of NF-κB p65 and inflammatory cytokines expression in cardiomyocytes. Furthermore, inflammation response emerged in macrophages cultured in cardiomyocytes-conditioned medium. When pretreatment with 14,15-EET in cardiomyocytes, the inflammatory response was markedly suppressed and the transmission of inflammation from cardiomyocytes to macrophages was reduced. In conclusion, CYP2J2 and EETs prevent cardiac fibrosis and cardiac dysfunction by suppressing transmission of pro-inflammation from cardiomyocytes to macrophages in heart, suggesting that elevation of EETs level could be a potential strategy to prevent cardiac fibrosis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Prostaglandins & Other Lipid Mediators - Volumes 116â117, JanuaryâMarch 2015, Pages 64-75
Journal: Prostaglandins & Other Lipid Mediators - Volumes 116â117, JanuaryâMarch 2015, Pages 64-75
نویسندگان
Lei Yang, Li Ni, Quanlu Duan, Xingxu Wang, Chen Chen, Song Chen, Sandip Chaugai, D.C. Zeldin, Jia Rong Tang, Dao Wen Wang,