کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10752811 | 1050332 | 2015 | 7 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Inhibition of osteoclastogenesis by osteoblast-like cells genetically engineered to produce interleukin-10
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کلمات کلیدی
BSPOPNOCNRheumatoid arthritis - آرتریتروماتوئیدALP - آلکالن فسفاتازAlkaline phosphatase - آلکالین فسفاتاز یا فسفاتاز قلیاییOsteoblast - استئوبلاست Osteopontin - استئوپنتینOsteocalcin - استئوکلسین inflammation - التهاب( توروم) Interleukin-10 - اینترلوکین 10bone sialoprotein - سیلوپروتئین استخوانGene therapy - ژن درمانی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
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چکیده انگلیسی
Bone destruction at inflamed joints is an important complication associated with rheumatoid arthritis (RA). Interleukin-10 (IL-10) may suppress not only inflammation but also induction of osteoclasts that play key roles in the bone destruction. If IL-10-producing osteoblast-like cells are induced from patient somatic cells and transplanted back into the destructive bone lesion, such therapy may promote bone remodeling by the cooperative effects of IL-10 and osteoblasts. We transduced mouse fibroblasts with genes for IL-10 and Runx2 that is a crucial transcription factor for osteoblast differentiation. The IL-10-producing induced osteoblast-like cells (IL-10-iOBs) strongly expressed osteoblast-specific genes and massively produced bone matrix that were mineralized by calcium phosphate in vitro and in vivo. Culture supernatant of IL-10-iOBs significantly suppressed induction of osteoclast from RANKL-stimulated Raw264.7 cells as well as LPS-induced production of inflammatory cytokine by macrophages. The IL-10-iOBs may be applicable to novel cell-based therapy against bone destruction associated with RA.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochemical and Biophysical Research Communications - Volume 456, Issue 3, 16 January 2015, Pages 785-791
Journal: Biochemical and Biophysical Research Communications - Volume 456, Issue 3, 16 January 2015, Pages 785-791
نویسندگان
Kazuki Fujioka, Tsunao Kishida, Akika Ejima, Kenta Yamamoto, Wataru Fujii, Ken Murakami, Takahiro Seno, Aihiro Yamamoto, Masataka Kohno, Ryo Oda, Toshiro Yamamoto, Hiroyoshi Fujiwara, Yutaka Kawahito, Osam Mazda,