14-3-3η inhibits chondrogenic differentiation of ATDC5 cell

Hee Eun Yoon; Ki Soon Kim; Ick Young Kim

doi:10.1016/j.bbrc.2011.01.107

14-3-3η inhibits chondrogenic differentiation of ATDC5 cell

Hee Eun Yoon, Ki Soon Kim, Ick Young Kim

Department of Life Sciences

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

Abstract

It was previously shown that 14-3-3η is overexpressed in the synovial fluid of patients with joint inflammation, which is often associated with growth failure. In this study, we investigated the role of 14-3-3η in chondrogenesis using ATDC5 cells. Upon treatment with TNF-α, cells overexpressed 14-3-3η with inhibition of chondrogenesis. Chondrogenesis was also inhibited by overexpression of 14-3-3η without TNF-α treatment, whereas silencing of 14-3-3η promoted chondrogenic differentiation. Further, G1 phase arrest was inhibited by overexpression of 14-3-3η. In summary, we suggest that 14-3-3η plays a regulatory role in chondrogenic differentiation.

Original language	English
Pages (from-to)	59-63
Number of pages	5
Journal	Biochemical and biophysical research communications
Volume	406
Issue number	1
DOIs	https://doi.org/10.1016/j.bbrc.2011.01.107
Publication status	Published - 2011 Mar 4

Keywords

14-3-3η
ATDC5 cells
Chondrogenesis
Joint inflammation

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/j.bbrc.2011.01.107

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title = "14-3-3η inhibits chondrogenic differentiation of ATDC5 cell",

abstract = "It was previously shown that 14-3-3η is overexpressed in the synovial fluid of patients with joint inflammation, which is often associated with growth failure. In this study, we investigated the role of 14-3-3η in chondrogenesis using ATDC5 cells. Upon treatment with TNF-α, cells overexpressed 14-3-3η with inhibition of chondrogenesis. Chondrogenesis was also inhibited by overexpression of 14-3-3η without TNF-α treatment, whereas silencing of 14-3-3η promoted chondrogenic differentiation. Further, G1 phase arrest was inhibited by overexpression of 14-3-3η. In summary, we suggest that 14-3-3η plays a regulatory role in chondrogenic differentiation.",

keywords = "14-3-3η, ATDC5 cells, Chondrogenesis, Joint inflammation",

author = "Yoon, {Hee Eun} and Kim, {Ki Soon} and Kim, {Ick Young}",

note = "Funding Information: This research was supported by a National Research Foundation of Korea Grant funded by the Korean Government (Grant No. 2007-0053186 ). We thank Prof. J.S. Ko (Korea University) for kindly providing the plasmid expressing HA-14-3-3η. Copyright: Copyright 2011 Elsevier B.V., All rights reserved.",

year = "2011",

month = mar,

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doi = "10.1016/j.bbrc.2011.01.107",

language = "English",

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journal = "Biochemical and Biophysical Research Communications",

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AU - Yoon, Hee Eun

AU - Kim, Ki Soon

AU - Kim, Ick Young

N1 - Funding Information: This research was supported by a National Research Foundation of Korea Grant funded by the Korean Government (Grant No. 2007-0053186 ). We thank Prof. J.S. Ko (Korea University) for kindly providing the plasmid expressing HA-14-3-3η. Copyright: Copyright 2011 Elsevier B.V., All rights reserved.

PY - 2011/3/4

Y1 - 2011/3/4

N2 - It was previously shown that 14-3-3η is overexpressed in the synovial fluid of patients with joint inflammation, which is often associated with growth failure. In this study, we investigated the role of 14-3-3η in chondrogenesis using ATDC5 cells. Upon treatment with TNF-α, cells overexpressed 14-3-3η with inhibition of chondrogenesis. Chondrogenesis was also inhibited by overexpression of 14-3-3η without TNF-α treatment, whereas silencing of 14-3-3η promoted chondrogenic differentiation. Further, G1 phase arrest was inhibited by overexpression of 14-3-3η. In summary, we suggest that 14-3-3η plays a regulatory role in chondrogenic differentiation.

AB - It was previously shown that 14-3-3η is overexpressed in the synovial fluid of patients with joint inflammation, which is often associated with growth failure. In this study, we investigated the role of 14-3-3η in chondrogenesis using ATDC5 cells. Upon treatment with TNF-α, cells overexpressed 14-3-3η with inhibition of chondrogenesis. Chondrogenesis was also inhibited by overexpression of 14-3-3η without TNF-α treatment, whereas silencing of 14-3-3η promoted chondrogenic differentiation. Further, G1 phase arrest was inhibited by overexpression of 14-3-3η. In summary, we suggest that 14-3-3η plays a regulatory role in chondrogenic differentiation.

KW - 14-3-3η

KW - ATDC5 cells

KW - Chondrogenesis

KW - Joint inflammation

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14-3-3η inhibits chondrogenic differentiation of ATDC5 cell

Abstract

Keywords

ASJC Scopus subject areas

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