PMID- 20049872
OWN - NLM
STAT- MEDLINE
DCOM- 20100308
LR  - 20211203
IS  - 1097-4652 (Electronic)
IS  - 0021-9541 (Linking)
VI  - 223
IP  - 1
DP  - 2010 Apr
TI  - NF-kappaB activation stimulates osteogenic differentiation of mesenchymal stem 
      cells derived from human adipose tissue by increasing TAZ expression.
PG  - 168-77
LID - 10.1002/jcp.22024 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a skeletal catabolic agent that 
      stimulates osteoclastogenesis and inhibits osteoblast function. Although 
      TNF-alpha inhibits the mineralization of osteoblasts, the effect of TNF-alpha on 
      mesenchymal stem cells (MSC) is not clear. In this study, we determined the 
      effect of TNF-alpha on osteogenic differentiation of stromal cells derived from 
      human adipose tissue (hADSC) and the role of NF-kappaB activation on TNF-alpha 
      activity. TNF-alpha treatment dose-dependently increased osteogenic 
      differentiation over the first 3 days of treatment. TNF-alpha activated ERK and 
      increased NF-kappaB promoter activity. PDTC, an NF-kappaB inhibitor, blocked the 
      osteogenic differentiation induced by TNF-alpha and TLR-ligands, but U102, an ERK 
      inhibitor, did not. Overexpression of miR-146a induced the inhibition of IRAK1 
      expression and inhibited basal and TNF-alpha- and TLR ligand-induced osteogenic 
      differentiation. TNF-alpha and TLR ligands increased the expression of 
      transcriptional coactivator with PDZ-binding motif (TAZ), which was inhibited by 
      the addition of PDTC. A ChIP assay showed that p65 was bound to the TAZ promoter. 
      TNF-alpha also increased osteogenic differentiation of human gastroepiploic 
      artery smooth muscle cells. Our data indicate that TNF-alpha enhances osteogenic 
      differentiation of hADSC via the activation of NF-kappaB and a subsequent 
      increase of TAZ expression.
CI  - J. Cell. Physiol. 223: 168-177, 2010. (c) 2009 Wiley-Liss, Inc.
FAU - Cho, Hyun Hwa
AU  - Cho HH
AD  - Department of Physiology, School of Medicine, Pusan National University, Yangsan, 
      Korea.
FAU - Shin, Keun Koo
AU  - Shin KK
FAU - Kim, Yeon Jeong
AU  - Kim YJ
FAU - Song, Ji Sun
AU  - Song JS
FAU - Kim, Jong Myung
AU  - Kim JM
FAU - Bae, Yong Chan
AU  - Bae YC
FAU - Kim, Chi Dae
AU  - Kim CD
FAU - Jung, Jin Sup
AU  - Jung JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Physiol
JT  - Journal of cellular physiology
JID - 0050222
RN  - 0 (Butadienes)
RN  - 0 (MIRN146 microRNA, human)
RN  - 0 (MicroRNAs)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitriles)
RN  - 0 (Protein Kinase Inhibitors)
RN  - 0 (Pyrrolidines)
RN  - 0 (RELA protein, human)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Thiocarbamates)
RN  - 0 (Toll-Like Receptors)
RN  - 0 (Transcription Factor RelA)
RN  - 0 (Transcription Factors)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (U 0126)
RN  - 25769-03-3 (pyrrolidine dithiocarbamic acid)
RN  - EC 2.3.- (Acyltransferases)
RN  - EC 2.3.1.- (TAFAZZIN protein, human)
RN  - EC 2.7.11.1 (IRAK1 protein, human)
RN  - EC 2.7.11.1 (Interleukin-1 Receptor-Associated Kinases)
RN  - EC 2.7.11.24 (Extracellular Signal-Regulated MAP Kinases)
SB  - IM
MH  - Acyltransferases
MH  - Adipose Tissue/cytology/drug effects/*metabolism
MH  - Binding Sites
MH  - Butadienes/pharmacology
MH  - Calcinosis/metabolism/pathology
MH  - *Cell Differentiation/drug effects
MH  - Cells, Cultured
MH  - Enzyme Activation
MH  - Extracellular Signal-Regulated MAP Kinases/antagonists & inhibitors/metabolism
MH  - Female
MH  - Humans
MH  - Interleukin-1 Receptor-Associated Kinases/metabolism
MH  - Male
MH  - Mesenchymal Stem Cells/drug effects/*metabolism
MH  - MicroRNAs/metabolism
MH  - Middle Aged
MH  - Muscle, Smooth, Vascular/metabolism/pathology
MH  - Myocytes, Smooth Muscle/metabolism/pathology
MH  - NF-kappa B/antagonists & inhibitors/genetics/*metabolism
MH  - Nitriles/pharmacology
MH  - *Osteogenesis/drug effects
MH  - Promoter Regions, Genetic
MH  - Protein Kinase Inhibitors/pharmacology
MH  - Pyrrolidines/pharmacology
MH  - RNA Interference
MH  - Recombinant Proteins/metabolism
MH  - Thiocarbamates/pharmacology
MH  - Time Factors
MH  - Toll-Like Receptors/metabolism
MH  - Transcription Factor RelA/metabolism
MH  - Transcription Factors/genetics/*metabolism
MH  - Transfection
MH  - Tumor Necrosis Factor-alpha/metabolism
MH  - Up-Regulation
EDAT- 2010/01/06 06:00
MHDA- 2010/03/10 06:00
CRDT- 2010/01/06 06:00
PHST- 2010/01/06 06:00 [entrez]
PHST- 2010/01/06 06:00 [pubmed]
PHST- 2010/03/10 06:00 [medline]
AID - 10.1002/jcp.22024 [doi]
PST - ppublish
SO  - J Cell Physiol. 2010 Apr;223(1):168-77. doi: 10.1002/jcp.22024.