PMID- 25350220
OWN - NLM
STAT- MEDLINE
DCOM- 20160204
LR  - 20181202
IS  - 1557-8534 (Electronic)
IS  - 1547-3287 (Linking)
VI  - 24
IP  - 7
DP  - 2015 Apr 1
TI  - Role of transforming growth factor-activated kinase-1 on tumor necrosis factor-alpha 
      actions in human adipose tissue-derived stromal cells.
PG  - 836-45
LID - 10.1089/scd.2014.0272 [doi]
AB  - Tumor necrosis factor-alpha (TNF-alpha) has multiple effects on proliferation and 
      differentiation of human mesenchymal stem cells. Transforming growth 
      factor-activated kinase-1 (TAK1) mediates the activation of nuclear factor-kappa 
      B (NF-kappaB), c-Jun N-terminal kinase (JNK), and p38 pathways in response to TNF-alpha. 
      However, the role of TAK1 in TNF-alpha-induced effects in human adipose-derived stem 
      cells (hADSCs) and its signaling pathway has not been clearly defined. Therefore, 
      this study was designated to clarify the role of TAK1 in TNF-alpha-induced actions on 
      proliferation and differentiation of hADSCs and its downstream signaling pathway. 
      Inhibiting TAK1 expression inhibited the TNF-alpha-induced increase in osteogenic 
      differentiation and basal osteogenic differentiation without affecting the 
      TNF-alpha-induced effect on proliferation and adipogenic differentiation of hADSCs. A 
      western blot analysis showed that TNF-alpha treatment induced degradation of IkappaB, but 
      that TAK1 small interfering RNA (siRNA) transfection did not protect against 
      TNF-alpha-induced IkappaB degradation. The transfection of TAK1 siRNA also did not affect 
      TNF-alpha-induced IkappaB phosphorylation or ERK1/2 phosphorylation. However, 
      downregulating TAK1 inhibited this TNF-alpha-induced S536 phosphorylation of the p65 
      subunit. TNF-alpha treatment induced p38 phosphorylation, which was inhibited by the 
      transfection of TAK1 siRNA. Adding p38 inhibitor inhibited TNF-alpha-induced p65 
      phosphorylation, NF-kappaB promoter activity, and TNF-alpha-induced increase in hADSC 
      osteogenic differentiation. These data indicate that TAK1 is involved in the 
      TNF-alpha-induced activation of p38 kinase, which subsequently phosphorylates the 
      NF-kappaB p65 subunit, and increases the transactivation potential of p65 and 
      osteogenic differentiation in hADSCs.
FAU - Lee, Sun Young
AU  - Lee SY
AD  - 1 Department of Physiology, School of Medicine, Pusan National University , 
      Yangsan, Gyeongnam, Korea.
FAU - Lee, Jung Hee
AU  - Lee JH
FAU - Shin, Keun Koo
AU  - Shin KK
FAU - Kim, Da Sol
AU  - Kim DS
FAU - Kim, Young Suk
AU  - Kim YS
FAU - Bae, Yong Chan
AU  - Bae YC
FAU - Jung, Jin Sup
AU  - Jung JS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20141231
PL  - United States
TA  - Stem Cells Dev
JT  - Stem cells and development
JID - 101197107
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.25 (MAP Kinase Kinase Kinases)
RN  - EC 2.7.11.25 (MAP kinase kinase kinase 7)
SB  - IM
MH  - Adipose Tissue/*cytology
MH  - Adult
MH  - *Cell Differentiation
MH  - Cell Proliferation
MH  - Cells, Cultured
MH  - Female
MH  - Humans
MH  - MAP Kinase Kinase Kinases/genetics/*metabolism
MH  - Male
MH  - Mesenchymal Stem Cells/*cytology/drug effects/metabolism/physiology
MH  - Middle Aged
MH  - Mitogen-Activated Protein Kinase 1/metabolism
MH  - Mitogen-Activated Protein Kinase 3/metabolism
MH  - NF-kappa B/metabolism
MH  - Tumor Necrosis Factor-alpha/*pharmacology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2014/10/29 06:00
MHDA- 2016/02/05 06:00
CRDT- 2014/10/29 06:00
PHST- 2014/10/29 06:00 [entrez]
PHST- 2014/10/29 06:00 [pubmed]
PHST- 2016/02/05 06:00 [medline]
AID - 10.1089/scd.2014.0272 [doi]
PST - ppublish
SO  - Stem Cells Dev. 2015 Apr 1;24(7):836-45. doi: 10.1089/scd.2014.0272. Epub 2014 
      Dec 31.