کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5506137 | 1400287 | 2017 | 23 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Ameloblastin and enamelin prevent osteoclast formation by suppressing RANKL expression via MAPK signaling pathway
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کلمات کلیدی
DEX1,25-Dihydroxy-vitamin D3Jun amino-terminal kinasesBMCsOPGα-MEMTRAPRANKLJnk1,25(OH)2D3 - 1،25 (OH) 2D3ERK1/2 - ERK1 / 2MAPK - MAPKAmeloblastin - آملوبلاستینtartrate-resistant acid phosphatase - اسید فسفاتاز مقاوم در برابر تارتاتDexamethasone - دگزامتازونBone marrow-derived macrophages - ماکروفاژها حاصل از استخوان مغز استخوانEnamelin - میناmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenreceptor activator of nuclear factor kappa-B ligand - گیرنده گیرنده لیگاند کاپا-B فاکتور هسته ای
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Ameloblastin (Ambn) and enamelin (Enam) play a pivotal role in enamel mineralization. Previous studies have demonstrated that these enamel-related gene products also affect bone growth and remodeling; however, the underlying mechanisms have not been elucidated. In the present study, we examined the effects of Ambn and Enam on the receptor activator of nuclear factor kappa-B ligand (RANKL) expression induced with 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) and dexamethasone (DEX) on mouse bone marrow stromal cell line ST2 cells. We then verified the effect of Ambn and Enam on osteoclastogenesis. We found that pretreatment with recombinant human Ambn (rhAmbn) and recombinant human Enam (rhEnam) remarkably suppressed RANKL mRNA and protein expression induced with 1,25(OH)2D3 and DEX. Interestingly, rhAmbn and rhEnam attenuated the phosphorylation of mitogen-activated protein kinases (MAPK), including ERK1/2, JNK, and p38 in ST2 cells stimulated with 1,25(OH)2D3 and DEX. Moreover, pretreatment with specific inhibitors of ERK1/2 and p38, but not JNK, blocked RANKL mRNA and protein expression. Cell co-culture results showed that rhAmbn and rhEnam downregulated mouse bone marrow cell differentiation into osteoclasts induced with 1,25(OH)2D3 and DEX-stimulated ST2 cells. These results suggest that Ambn and Enam may indirectly suppress RANKL-induced osteoclastogenesis via downregulation of p38 and ERK1/2 MAPK signaling pathways in bone marrow stromal cells.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 485, Issue 3, 8 April 2017, Pages 621-626
Journal: Biochemical and Biophysical Research Communications - Volume 485, Issue 3, 8 April 2017, Pages 621-626
نویسندگان
Wichida Chaweewannakorn, Wataru Ariyoshi, Toshinori Okinaga, Kazumasa Morikawa, Katsura Saeki, Kenshi Maki, Tatsuji Nishihara,