Regulation of chondrocytic phenotype by micro RNA 18a: Involvement of Ccn2/Ctgf as a major target gene

We searched for miRNAs that were down-regulated in chondrocytic cells and predicted to target CCN2/connective tissue growth factor (CCN2/CTGF) that promotes endochondral ossification. Among them, expression of miR-18a was most strongly repressed in chondrocytic cells. Reporter gene analysis confirme...

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Bibliographic Details
Published in:FEBS letters 2009-03, Vol.583 (6), p.1006-1010
Main Authors: Ohgawara, Toshihiro, Kubota, Satoshi, Kawaki, Harumi, Kondo, Seiji, Eguchi, Takanori, Kurio, Naito, Aoyama, Eriko, Sasaki, Akira, Takigawa, Masaharu
Format: Article
Language:English
Subjects:
Animals
Base Sequence
CCN family
Cell Differentiation - genetics
Cells, Cultured
Chickens
Chondrocyte
Chondrocytes - metabolism
Chondrocytes - physiology
Chondrogenesis - genetics
Connective tissue growth factor
Connective Tissue Growth Factor - genetics
Connective Tissue Growth Factor - metabolism
Connective Tissue Growth Factor - physiology
Gene Expression Profiling
Gene Expression Regulation
HeLa Cells
Humans
Micro RNA
MicroRNAs - genetics
MicroRNAs - metabolism
MicroRNAs - physiology
miR-18a
Oligonucleotide Array Sequence Analysis
Phenotype
Regulatory Elements, Transcriptional
Sequence Homology, Nucleic Acid
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Summary:We searched for miRNAs that were down-regulated in chondrocytic cells and predicted to target CCN2/connective tissue growth factor (CCN2/CTGF) that promotes endochondral ossification. Among them, expression of miR-18a was most strongly repressed in chondrocytic cells. Reporter gene analysis confirmed the functionality of an miR-18a target in the 3′-untranslated region of Ccn2 mRNA, which was predicted in silico. Indeed, introduction of miR-18a efficiently repressed the CCN2 production from chondrocytic cells. Finally, transfected miR-18a significantly repressed the mature chondrocytic phenotype. Our present study revealed a regulatory role for miR-18a in chondrocytic differentiation through CCN2.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2009.02.025