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Published in: International Orthopaedics 5/2013

01-05-2013 | Original Paper

Down-regulation of programmed cell death 5 by insulin-like growth factor 1 in osteoarthritis chondrocytes

Authors: Chengqing Yi, Chunhui Ma, Zongping Xie, Guoqiao Zhang, Wangsheng Song, Xiaokai Zhou, Yun Cao

Published in: International Orthopaedics | Issue 5/2013

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Abstract

Purpose

The aim of this study was to investigate the expression of insulin-like growth factor (IGF)-1 and programmed cell death 5 (PDCD5) in osteoarthritis chondrocytes, and to explore the potential correlation between them in the apoptosis process of osteoarthritis chondrocytes.

Methods

Patients with knee osteoarthritis were placed into four categories according to radiological staging. The mRNA and protein levels of IGF-1 and PDCD5 in osteoarthritis chondrocytes were respectively detected by quantitative reverse transcriptase polymerase chain reaction (qPCR) and western blotting. In addition, IGF-1 and PDCD5 protein expression in chondrocytes were also measured by immunohistochemistry. Apoptotic cells were measured by TUNEL staining.

Results

Both the mRNA and protein levels of IGF-1 were down-regulated, while the levels of PDCD5 were up-regulated, and the mRNA and protein levels of IGF-1 were negatively correlated with those of PDCD5, respectively. The apoptotic cell was significantly increased in osteoarthritis chondrocytes compared with control. Importantly, the apoptosis rate was positively correlated with PDCD5 protein expression and negatively correlated with IGF-1 protein expression

Conclusions

We concluded that IGF-1 may down-regulate the expression of PDCD5 and thus inhibit the apoptosis of osteoarthritis chondrocytes.
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Metadata
Title
Down-regulation of programmed cell death 5 by insulin-like growth factor 1 in osteoarthritis chondrocytes
Authors
Chengqing Yi
Chunhui Ma
Zongping Xie
Guoqiao Zhang
Wangsheng Song
Xiaokai Zhou
Yun Cao
Publication date
01-05-2013
Publisher
Springer-Verlag
Published in
International Orthopaedics / Issue 5/2013
Print ISSN: 0341-2695
Electronic ISSN: 1432-5195
DOI
https://doi.org/10.1007/s00264-012-1744-x

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