A1 Refereed original research article in a scientific journal
MicroRNAs Regulate Osteogenesis and Chondrogenesis of Mouse Bone Marrow Stromal Cells
Authors: Suomi S, Taipaleenmaki H, Seppanen A, Ripatti T, Vaananen K, Hentunen T, Saamanen AM, Laitala-Leinonen T
Publisher: SAGE PUBLICATIONS LTD
Publication year: 2008
Journal: Gene Regulation and Systems Biology
Journal name in source: GENE REGULATION AND SYSTEMS BIOLOGY
Journal acronym: GENE REGUL SYST BIO
Volume: 2
First page : 177
Last page: 191
Number of pages: 15
ISSN: 1177-6250
Abstract
MicroRNAs (miRNAs) are non-coding RNAs that bind to target mRNA leading to translational arrest or mRNA degradation. To study miRNA-mediated regulation of osteogenesis and chondrogenesis, we compared the expression of 35 miRNAs in osteoblasts and chondroblasts derived from mouse marrow stromal cells (MSCs). Differentiation of MSCs resulted in up-or downregulation of several miRNAs, with miR-199a expression being over 10-fold higher in chondroblasts than in undifferentiated MSCs. In addition, miR-124a was strongly upregulated during chondrogenesis while the expression of miR-96 was substantially suppressed. A systems biological analysis of the potential miRNA target genes and their interaction networks was combined with promoter analysis. These studies link the differentially expressed miRNAs to collagen synthesis and hypoxia, key pathways related to bone and cartilage physiology. The global regulatory networks described here suggest for the fi rst time how miRNAs and transcription factors are capable of fi ne-tuning the osteogenic and chondrogenic differentiation of mouse MSCs.
MicroRNAs (miRNAs) are non-coding RNAs that bind to target mRNA leading to translational arrest or mRNA degradation. To study miRNA-mediated regulation of osteogenesis and chondrogenesis, we compared the expression of 35 miRNAs in osteoblasts and chondroblasts derived from mouse marrow stromal cells (MSCs). Differentiation of MSCs resulted in up-or downregulation of several miRNAs, with miR-199a expression being over 10-fold higher in chondroblasts than in undifferentiated MSCs. In addition, miR-124a was strongly upregulated during chondrogenesis while the expression of miR-96 was substantially suppressed. A systems biological analysis of the potential miRNA target genes and their interaction networks was combined with promoter analysis. These studies link the differentially expressed miRNAs to collagen synthesis and hypoxia, key pathways related to bone and cartilage physiology. The global regulatory networks described here suggest for the fi rst time how miRNAs and transcription factors are capable of fi ne-tuning the osteogenic and chondrogenic differentiation of mouse MSCs.
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