Vaspin Attenuates RANKL-Induced Osteoclast Formation in RAW264.7 Cells

Visceral adipose tissue-derived serine protease inhibitor (vaspin), an adipokine that was recently identified in a rat model of type 2 diabetes, has been suggested to have an insulin-sensitizing effect. In this study, we investigated whether vaspin inhibits receptor activator of nuclear factor-κB li...

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Bibliographic Details
Published in:Connective tissue research 2013-04, Vol.54 (2), p.147-152
Main Authors: Kamio, Noriaki, Kawato, Takayuki, Tanabe, Natsuko, Kitami, Satoshi, Morita, Toyoko, Ochiai, Kuniyasu, Maeno, Masao
Format: Article
Language:English
Subjects:
adipokine
Adipokines - metabolism
Animals
Bone Marrow Cells - drug effects
Bone Marrow Cells - metabolism
cathepsin K
Cathepsin K - metabolism
Cell Line
Humans
Matrix Metalloproteinase 9 - metabolism
Mice
MMP-9
NFATC Transcription Factors - metabolism
NFATc1
osteoclastogenesis
Osteoclasts - cytology
Osteoclasts - drug effects
Osteoclasts - enzymology
Osteoclasts - metabolism
RANK Ligand - pharmacology
Rats
Serpins - metabolism
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Summary:Visceral adipose tissue-derived serine protease inhibitor (vaspin), an adipokine that was recently identified in a rat model of type 2 diabetes, has been suggested to have an insulin-sensitizing effect. In this study, we investigated whether vaspin inhibits receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis using two types of osteoclast precursors: RAW264.7 cells and bone marrow cells (BMCs). Vaspin inhibited RANKL-induced osteoclastogenesis in RAW264.7 cells and BMCs. Interestingly, vaspin also inhibited the RANKL-induced expression of nuclear factor of activated T cells c1 (NFATc1) in RAW264.7 cells and BMCs. Furthermore, it inhibited the RANKL-induced upregulation of matrix metalloproteinase-9 and cathepsin K in RAW264.7 cells. Thus, we suggest that vaspin downregulates osteoclastogenesis in part by inhibiting expression of the transcription factor NFATc1.
ISSN:0300-8207
1607-8438
DOI:10.3109/03008207.2012.761978