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Role of IRAK1 on TNF-induced proliferation and NF-ĸB activation in human bone marrow mesenchymal stem cells

Authors
Kim, JM; Cho, HH; Lee, SY; Hong, CP; Yang, Jw; Kim, YS; Suh, KT; Jung, JS
Citation
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology, 30(1):49-60, 2012
Journal Title
Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology
ISSN
1015-89871421-9778
Abstract
In this study, we determined the effect of TNF-α on hBMSCs proliferation as well as the role of IL-1 receptor-associated kinase 1 (IRAK1) on TNF-α signaling. Western blot analysis revealed that TNF-α treatment increased the phosphorylation of IRAK1 in hBMSCs. The downregulation of IRAK1 inhibited TNF-α-induced NF-ĸB activation and COX-2 expression. TNF-α treatment increased hBMSCs proliferation in a dose-dependent manner and increased ERK, JNK, and NF-ĸB activity. U0126, an ERK inhibitor, decreased hBMSCs proliferation and significantly blocked TNF-α -induced hBMSCs proliferation. In cells with IRAK1 or TRADD downregulation, the U0126 treatment inhibited hBMSCs proliferation and significantly suppressed TNF-α-induced hBMSCs proliferation. The downregulation of IRAK1 or TRADD inhibited TNF-α-induced ERK and JNK activation, and hBMSCs proliferation. Inhibition of NF-ĸB by decoy oligonucleotides reduced the TNF-α-induced hBMSCs proliferation. Immunoprecipitation analysis showed that IRAK1 does not physically interact with TNF receptor 1 (TNFR1) even in the presence of TNF-α. Suppression of IRAK1 binding protein (IRAK1BP1) inhibited TNF-α-induced increase of the proliferation and ERK1 phosphorylation of hBMSCs in the presence of TNF-α. Our data indicate that TNF-α modulates hBMSCs proliferation through ERK signaling pathways, and that IRAK1 plays an important role in TNF-α-induced NF-ĸB activation in hBMSCs.
MeSH terms
Bone Marrow Cells/*metabolism/physiology*Cell ProliferationCells, CulturedCyclooxygenase 2/genetics/metabolismFemaleGene Knockdown TechniquesHumansInterleukin-1 Receptor-Associated Kinases/genetics/metabolism/*physiologyMAP Kinase Signaling SystemMaleMesenchymal Stromal Cells/*metabolism/physiologyMiddle AgedMitogen-Activated Protein Kinases/antagonists & inhibitors/metabolismNF-kappa B/antagonists & inhibitors/metabolismOligodeoxyribonucleotides/pharmacologyProtein Kinase Inhibitors/pharmacologyRNA InterferenceReceptors, Tumor Necrosis Factor, Type I/metabolismTNF Receptor-Associated Death Domain Protein/genetics/metabolismTumor Necrosis Factor-alpha/*physiology
DOI
10.1159/000339045
PMID
22759955
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
AJOU Authors
김, 유선
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