کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8292241 | 1536726 | 2018 | 6 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Necrostatin-7 suppresses RANK-NFATc1 signaling and attenuates macrophage to osteoclast differentiation
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کلمات کلیدی
IκBαAtp6v0d2Acp5nuclear factor of activated T cells c1CTSKNFATc1M-CSFNecrostatinNF-κBNECTRAPJnkBMMERKRANKLc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKOsteoclast - استخوانکاه، استئوکلاستtartrate-resistant acid phosphatase - اسید فسفاتاز مقاوم در برابر تارتاتRank - رتبهNuclear factor-kappa B - فاکتور هسته ای-کاپا BRANK ligand - لیگاند RANKMacrophage - ماکروفاژ bone marrow-derived macrophage - ماکروفاژ حاصل از مغز استخوانmacrophage colony-stimulating factor - ماکروفاژ عامل کلونی تحریک کنندهmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenCathepsin K - کتهفسین کextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Necrostatin-7 suppresses RANK-NFATc1 signaling and attenuates macrophage to osteoclast differentiation Necrostatin-7 suppresses RANK-NFATc1 signaling and attenuates macrophage to osteoclast differentiation](/preview/png/8292241.png)
چکیده انگلیسی
Osteoclasts play a crucial role in osteolytic bone diseases, such as osteoporosis, rheumatoid arthritis, periodontitis, Paget's disease of bone and bone metastatic tumors. Therefore, controlling osteoclast differentiation and function has been considered a promising therapeutic strategy. Here, we show that necrostatin (Nec)-7, an inhibitor of programmed necrosis, strongly suppressed receptor activator of nuclear factor (NF)-κB ligand (RANKL)-induced osteoclastogenesis and bone resorption, without compromising macrophage colony-stimulating factor (M-CSF)-supported survival and growth of osteoclast precursor cells. Accordingly, Nec-7 significantly decreased the levels of RANKL-induced osteoclastogenic marker genes, such as cathepsin K. Mechanistically, Nec-7 neither affected MAPK nor NF-κB activation; however, it strongly inhibited the RANKL receptor (RANK) to nuclear factor of activated T cells c1 (NFATc1) signaling. Lentiviral expression of RANK in bone marrow-derived macrophages significantly restored osteoclastogenesis and NFATc1 amplification in Nec-7-treated cells. In this study, we revealed that Nec-7-sensitive pathways are crucially involved in osteoclast formation and function. Investigation of the molecular mechanism(s) through which Nec-7 inhibits RANK-NFATc1 signaling axis may lead to the development of new therapeutic strategies for bone disease.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 503, Issue 2, 5 September 2018, Pages 544-549
Journal: Biochemical and Biophysical Research Communications - Volume 503, Issue 2, 5 September 2018, Pages 544-549
نویسندگان
Hiroaki Fuji, Saori Ohmae, Naruto Noma, Masatoshi Takeiri, Hideto Yasutomi, Kazuya Izumi, Moe Ito, Masayasu Toyomoto, Soichiro Iwaki, Kenji Takemoto, Satoru Seo, Kojiro Taura, Shigeaki Hida, Mineyoshi Aoyama, Yasushi Ishihama, Masatoshi Hagiwara,