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Published in: International Orthopaedics 12/2015

01-12-2015 | Original Paper

The impact of hypoxia on mesenchymal progenitor cells of human skeletal tissue in the pathogenesis of heterotopic ossification

Authors: Sebastian Winkler, Tanja Niedermair, Bernd Füchtmeier, Joachim Grifka, Susanne Grässel, Sven Anders, Guido Heers, Ferdinand Wagner

Published in: International Orthopaedics | Issue 12/2015

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Abstract

Purpose

Mesenchymal progenitor cells (MPCs) are capable of differentiating into osteo/chondrogenic cells to contribute substantially to heterotopic ossification (HO). This study aimed to examine the impact of hypoxia on MPCs in the aetiology of HO.

Methods

MPCs from human normal and HO skeletal tissue were cultivated under normoxia and hypoxia. Gene expression of factors which have a key role in HO aetiology (BMPs, COX-1 and COX-2, etc.) were examined by real-time PCR. Tissue of both groups was analysed by immunohistochemistry.

Results

Under hypoxia, COX-1, -2 and SOX-9 gene expression was elevated in HO MPCs, whereas in normal muscle tissue only COX-2 was upregulated. MPCs from HO had a significantly elevated gene expression of BMP-4 and decreased expression of BMP-1 and HIF-1 under hypoxia compared to normal MPCs. Immunohistochemistry detected no significant differences between normal and HO tissue.

Conclusions

Hypoxia causes an enhanced gene expression of factors, which have a key role in HO pathophysiology. A better understanding of this entity will possibly allow reducing HO rates in orthopaedic and trauma surgery.
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Metadata
Title
The impact of hypoxia on mesenchymal progenitor cells of human skeletal tissue in the pathogenesis of heterotopic ossification
Authors
Sebastian Winkler
Tanja Niedermair
Bernd Füchtmeier
Joachim Grifka
Susanne Grässel
Sven Anders
Guido Heers
Ferdinand Wagner
Publication date
01-12-2015
Publisher
Springer Berlin Heidelberg
Published in
International Orthopaedics / Issue 12/2015
Print ISSN: 0341-2695
Electronic ISSN: 1432-5195
DOI
https://doi.org/10.1007/s00264-015-2995-0

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