کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8474149 | 1550419 | 2015 | 10 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The mammalian target of rapamycin modulates the immunoproteasome system in the heart
ترجمه فارسی عنوان
هدف پستانداران رپامایسین سیستم ایمنی بدن را در قلب متصل می کند
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کلمات کلیدی
NF-κBmTORLMPSTAT1/3inflammation - التهاب( توروم) Immunoproteasome - ایمونو پروتئازومRapamycin - راپامایسینUbiquitin proteasome system - سیستم پروتئازوم UbiquitinNuclear factor κ B - عامل هسته ای κ BHeart - قلب mammalian target of rapamycin - هدف پستانداران رپامایسینProteasome - پروتئازومUPS - یو پی اس
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
بیولوژی سلول
چکیده انگلیسی
The mammalian target of rapamycin (mTOR) plays an important role in cardiac development and function. Inhibition of mTOR by rapamycin has been shown to attenuate pathological cardiac hypertrophy and improve the function of aging heart, accompanied by an inhibition of the cardiac proteasome activity. The current study aimed to determine the potential mechanism(s) by which mTOR inhibition modulates cardiac proteasome. Inhibition of mTOR by rapamycin was found to reduce primarily the immunoproteasome in both H9c2 cells in vitro and mouse heart in vivo, without significant effect on the constitutive proteasome and protein ubiquitination. Concurrent with the reduction of the immunoproteasome, rapamycin reduced two important inflammatory response pathways, the NF-κB and Stat3 signaling. In addition, rapamycin attenuated the induction of the immunoproteasome in H9c2 cells by inflammatory cytokines, including INFγ and TNFα, by suppressing NF-κB signaling. These data indicate that rapamycin indirectly modulated immunoproteasome through the suppression of inflammatory response pathways. Lastly, the role of the immunoproteasome during the development of cardiac hypertrophy was investigated. Administration of a specific inhibitor of the immunoproteasome ONX 0914 attenuated isoproterenol-induced cardiac hypertrophy, suggesting that the immunoproteasome may be involved in the development of cardiac hypertrophy and therefore could be a therapeutic target. In conclusion, rapamycin inhibits the immunoproteasome through its effect on the inflammatory signaling pathways and the immunoproteasome could be a potential therapeutic target for pathological cardiac hypertrophy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Journal of Molecular and Cellular Cardiology - Volume 86, September 2015, Pages 158-167
Journal: Journal of Molecular and Cellular Cardiology - Volume 86, September 2015, Pages 158-167
نویسندگان
Hong-Mei Zhang, Jianliang Fu, Ryan Hamilton, Vivian Diaz, Yiqiang Zhang,