کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5917549 | 1570737 | 2011 | 12 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Free heme is a danger signal inducing expression of proinflammatory proteins in cultured cells derived from normal rat hearts
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کلمات کلیدی
TLCKTPCKCCRCLCN2IL-1Heme oxygenase-1RASMCHO-1RCFEAM - POMROS - ROSinflammation - التهاب( توروم) interleukin-1 - اینترلوکین-1Tosyl phenylalanyl chloromethyl ketone - تسیل فنیل آلانیل کلرومتیل کتونOxidative stress - تنش اکسیداتیوRat aortic smooth muscle cells - سلول های عضلانی صاف آئورت موشCytokines - سیتوکین هاlipocalin-2 - لیپوکالین-2Macrophages - ماکروفاژها،درشت خوارهاexperimental autoimmune myocarditis - میوکاردیت خود ایمنی تجربیCRC - کد افزونگی دورهای Chemokines - کرموین هاReactive oxygen species - گونههای فعال اکسیژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شناسی مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Free heme is a danger signal inducing expression of proinflammatory proteins in cultured cells derived from normal rat hearts Free heme is a danger signal inducing expression of proinflammatory proteins in cultured cells derived from normal rat hearts](/preview/png/5917549.png)
چکیده انگلیسی
Endogenous molecules from damaged tissue act as danger signals to trigger or amplify the immune/inflammatory response. In this study, we examined whether free heme induced pro-inflammatory proteins in cultured cells derived from normal hearts and investigated the cells targeted by heme, together with its mechanism of action in these cells. We cultured collagenase-isolated heart-derived cells from normal rats and examined whether free heme induced pro-inflammatory proteins, reactive oxygen species (ROS) production and NF-κB activation, by quantitative RT-PCR, ELISA and flow cytometry. Free heme increased mRNA of various pro-inflammatory proteins in cultured cardiac resident cells (CCRC) (at least 100-fold) and induced intracellular ROS formation. Approximately 85-90% of CCRC are fibroblast/smooth muscle cells and 10-15% are CD11bc-positive macrophages; therefore to examine individual target cells, macrophage-deleted (CD11bc-negative) CCRC, primary cultured cells (cardiac fibroblasts, arterial smooth muscle cells and cardiac microvascular endothelial cells) and macrophage cells lines (NR8383) were similarly treated. Free heme activated NF-κB and induced expression of some pro-inflammatory proteins, including IL-1 and TNF-α in NR8383. On the other hand, macrophage-deleted CCRC strongly increased expression of these proteins on treatment with IL-1 or TNF-α, but not free heme. Induction of expression of pro-inflammatory proteins by free heme was not inhibited by intracellular ROS reduction, but by protease and proteasome inhibitors capable of regulating NF-κB. These data suggest that free heme strongly induces various pro-inflammatory proteins in injured hearts through NF-κB activation in cardiac resident macrophages and through cross-talk between macrophages and fibroblast/smooth muscle cells mediated inter alia by IL-1, TNF-α.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Immunology - Volume 48, Issues 9â10, May 2011, Pages 1191-1202
Journal: Molecular Immunology - Volume 48, Issues 9â10, May 2011, Pages 1191-1202
نویسندگان
Kazuhisa Hao, Haruo Hanawa, Limin Ding, Yoshimi Ota, Kaori Yoshida, Ken Toba, Minako Ogura, Hiromi Ito, Makoto Kodama, Yoshifusa Aizawa,