کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474377 | 1550425 | 2015 | 36 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
NOR-1 modulates the inflammatory response of vascular smooth muscle cells by preventing NFκB activation
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کلمات کلیدی
eGFPnLDLMDANr4aoxLDLFCSTBARSDMEMOxidized LDL - LDL اکسید شدهMOI - MEDulbecco's modified Eagle's medium - Medal of Eagle اصلاح شده DulbeccoSmall interfering RNA - RNA تداخل کوچکsiRNA - siRNAElectrophoretic mobility shift assay - آزمون تحرک تحرک الکتروفورزfoetal calf serum - سرم گوساله جنینEndothelial cells - سلولهای اندوتلیالEMSA یا electrophoretic mobility shift assay - سنجش تغییر تحرک الکتروفورتیکmalondialdehyde - مالون دی آلدهیدthiobarbituric acid-reactive substances - مواد واکنش پذیر اسید تیوباربیتوریکenhanced green fluorescent protein - پروتئین فلورسنت سبز افزایش یافته استmultiplicity of infection - چندین عفونت
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: NOR-1 modulates the inflammatory response of vascular smooth muscle cells by preventing NFκB activation NOR-1 modulates the inflammatory response of vascular smooth muscle cells by preventing NFκB activation](/preview/png/8474377.png)
چکیده انگلیسی
Recent work has highlighted the role of NR4A receptors in atherosclerosis and inflammation. In vascular smooth muscle cell (VSMC) proliferation, however, NOR-1 (neuron-derived orphan receptor-1) exerts antagonistic effects to Nur77 and Nurr1. The aim of this study was to analyse the effect of NOR-1 in VSMC inflammatory response. We assessed the consequence of a gain-of-function of this receptor on the response of VSMC to inflammatory stimuli. In human VSMC, lentiviral over-expression of NOR-1 reduced lipopolysaccharide (LPS)-induced up-regulation of cytokines (IL-1β, IL-6 and IL-8) and chemokines (MCP-1 and CCL20). Similar effects were obtained in cells stimulated with TNFα or oxLDL. Conversely, siRNA-mediated NOR-1 inhibition significantly increased the expression of pro-inflammatory mediators. Interestingly, in the aortas from transgenic mice that over-express human NOR-1 in VSMC (TgNOR-1), the up-regulation of cytokine/chemokine by LPS was lower compared to wild-type littermates. Similar results were obtained in VSMC from transgenic animals. NOR-1 reduced the transcriptional activity of NFκB sensitive promoters (in transient transfections), and the binding of NFκB to its responsive element (in electrophoretic mobility shift assays). Furthermore, NOR-1 prevented the activation of NFκB pathway by decreasing IκBα phosphorylation/degradation and inhibiting the phosphorylation and subsequent translocation of p65 to the nucleus (assessed by Western blot and immunocytochemistry). These effects were associated with an attenuated phosphorylation of ERK1/2, p38 MAPK and Jun N-terminal kinase, pathways involved in the activation of NFκB. In mouse challenged with LPS, the activation of the NFκB signalling was also attenuated in the aorta from TgNOR-1. Our data support a role for NOR-1 as a negative modulator of the acute response elicited by pro-inflammatory stimuli in the vasculature.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 80, March 2015, Pages 34-44
Journal: Journal of Molecular and Cellular Cardiology - Volume 80, March 2015, Pages 34-44
نویسندگان
Olivier Calvayrac, Ricardo RodrÃguez-Calvo, Ingrid MartÃ-Pamies, Judith Alonso, Beatriz Ferrán, Silvia Aguiló, Javier Crespo, Antonio RodrÃguez-Sinovas, Cristina RodrÃguez, José MartÃnez-González,