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Open Access Research article

FGF2-induced effects on transcriptome associated with regeneration competence in adult human fibroblasts

Olga Kashpur1, David LaPointe2, Sakthikumar Ambady3, Elizabeth F Ryder1 and Tanja Dominko1*

Author Affiliations

1 Department of Biology and Biotechnology, Worcester Polytechnic Institute, 100 Institute Road, Worcester, MA 01609, USA

2 Department of Cell and Developmental Biology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA 01655, USA

3 Department of Biomedical Engineering, Worcester Polytechnic Institute, 100 Institute Road, Worcester, MA 01609, USA

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BMC Genomics 2013, 14:656  doi:10.1186/1471-2164-14-656

Published: 26 September 2013

Abstract

Background

Adult human fibroblasts grown in low oxygen and with FGF2 supplementation have the capacity to tip the healing outcome of skeletal muscle injury – by favoring regeneration response in vivo over scar formation. Here, we compare the transcriptomes of control adult human dermal fibroblasts and induced regeneration-competent (iRC) fibroblasts to identify transcriptional changes that may be related to their regeneration competence.

Results

We identified a unique gene-expression profile that characterizes FGF2-induced iRC fibroblast phenotype. Significantly differentially expressed genes due to FGF2 treatment were identified and analyzed to determine overrepresented Gene Ontology terms. Genes belonging to extracellular matrix components, adhesion molecules, matrix remodelling, cytoskeleton, and cytokines were determined to be affected by FGF2 treatment.

Conclusions

Transcriptome analysis comparing control adult human fibroblasts with FGF2-treated fibroblasts identified functional groups of genes that reflect transcriptional changes potentially contributing to their regeneration competence. This comparative transcriptome analysis should contribute new insights into genes that characterize cells with greater regenerative potential.

Keywords:
Transcriptome; Human fibroblasts; Fibroblast growth factor (FGF2); Wound healing; Regeneration