کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8303840 | 1537956 | 2013 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
IL-6 is produced by adipose-derived stromal cells and promotes osteogenesis
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کلمات کلیدی
STAT3osterixVon KossaTLRDAPIARSGAPDHMSCsIL-6LPSASCs4′,6-diamidino-2-phenylindole - 4 '، 6-دیامیدینو-2-فنیلینولSmall interfering RNA - RNA تداخل کوچکsIL-6R - SIL-6RsiRNA - siRNATLRs - TLR هاAlizarin red S - آلزارین قرمز SALP - آلکالن فسفاتازAlkaline phosphatase - آلکالین فسفاتاز یا فسفاتاز قلیاییOsteogenesis - استخوان زاییadipose-derived stromal cell - سلول استرومای حاصل از چربیAdipose-derived stromal cells - سلول های استرومای حاصل از چربیMesenchymal stem cells - سلول های بنیادی مزانشیمیlipopolysaccharide - لیپوپلی ساکاریدPolyinosinic:polycytidylic acid - پلی سونیک: پلیسییدیدیل اسیدglyceraldehyde 3 phosphate dehydrogenase - گلیسرولیدید 3 فسفات دهیدروژنازSoluble IL-6 receptor - گیرنده حلقوی IL-6Toll-like receptors - گیرنده های پولی مانند
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Although Toll-like receptors (TLRs) have been implicated in the regulation of stem cell functions, their role in osteogenic differentiation of adipose-derived stromal cells (ASCs) has not been reported. We found that ASCs express a restricted subset of TLRs, including TLR1-TLR5, and that TLR agonists such as Pam3CSK4 (TLR1/2 agonist), polyinosinic:polycytidylic acid (TLR3 agonist), lipopolysaccharide (TLR4 agonist), and flagellin (TLR5 agonist), but not R848 (TLR7/8 agonist), consistently induced osteogenic differentiation in murine-derived ASCs, which coincided with the TLR expression pattern of ASCs. Cytokine expression profiles induced by TLR agonists and results from subsequent functional assays indicated that interleukin-6 (IL-6) together with soluble IL-6 receptor (sIL-6R) enhanced osteogenic differentiation of ASCs by activating STAT3. Small interfering RNA (siRNA)-mediated STAT3-silencing blunted osteogenesis and the expression of osteogenic markers, whereas STAT3 overexpression resulted in an increase in osteogenesis. Consistently, STAT3 inhibitor treatment reduced osteogenesis, STAT3 phosphorylation, and expression of osteogenic markers including osterix. Chromatin immunoprecipitation (ChIP) assays indicated that STAT3 binding to the STAT3-binding sites on the osterix promoter increased during IL-6-stimulated osteogenesis. Our results thus establish TLRs as novel regulators of ASCs which signal through IL-6/STAT3 pathway and induce osterix expression as a part of the osteogenesis.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 12, December 2013, Pages 2608-2616
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Cell Research - Volume 1833, Issue 12, December 2013, Pages 2608-2616
نویسندگان
Jeong-Eun Huh, Soo Young Lee,