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IL-6 is produced by adipose-derived stromal cells and promotes osteogenesis

Title
IL-6 is produced by adipose-derived stromal cells and promotes osteogenesis
Authors
Huh J.-E.Lee S.Y.
Ewha Authors
이수영허정은
SCOPUS Author ID
이수영scopus; 허정은scopus
Issue Date
2013
Journal Title
Biochimica et Biophysica Acta - Molecular Cell Research
ISSN
0167-4889JCR Link
Citation
vol. 1833, no. 12, pp. 2608 - 2616
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
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. © 2013 Elsevier B.V.
DOI
10.1016/j.bbamcr.2013.06.025
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자연과학대학 > 생명과학전공 > Journal papers
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