miR-210 promotes osteoblastic differentiation through inhibition of AcvR1b

Although microRNAs (miRNAs) are involved in many biological processes, the mechanisms whereby miRNAs regulate osteoblastic differentiation are poorly understood. Here, we found that BMP-4-induced osteoblastic differentiation of bone marrow-derived ST2 stromal cells was promoted and repressed after t...

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Bibliographic Details
Published in:FEBS letters 2009-07, Vol.583 (13), p.2263-2268
Main Authors: Mizuno, Yosuke, Tokuzawa, Yoshimi, Ninomiya, Yuichi, Yagi, Ken, Yatsuka-Kanesaki, Yukiko, Suda, Tatsuo, Fukuda, Toru, Katagiri, Takenobu, Kondoh, Yasumitsu, Amemiya, Tomoyuki, Tashiro, Hideo, Okazaki, Yasushi
Format: Article
Language:English
Subjects:
Activin A receptor type 1B
Activin Receptors, Type I - antagonists & inhibitors
Activin Receptors, Type I - metabolism
activin-like kinase
AcvR1b
Alk
alkaline phosphatase
ALP
Animals
Bone Morphogenetic Protein 4 - metabolism
Cell Differentiation
Cells, Cultured
Differentiation
Mice
microRNA
MicroRNAs - metabolism
miR-210
miRNA
Osteoblast
Osteoblasts - cytology
Osteoblasts - metabolism
osteocalcin
Signal Transduction
TGF-β
Transfection
Transforming Growth Factor beta - metabolism
transforming growth factor-β
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Summary:Although microRNAs (miRNAs) are involved in many biological processes, the mechanisms whereby miRNAs regulate osteoblastic differentiation are poorly understood. Here, we found that BMP-4-induced osteoblastic differentiation of bone marrow-derived ST2 stromal cells was promoted and repressed after transfection of sense and antisense miR-210, respectively. A reporter assay demonstrated that the activin A receptor type 1B ( AcvR1b) gene was a target for miR-210. Furthermore, inhibition of transforming growth factor-β (TGF-β)/activin signaling in ST2 cells with SB431542 promoted osteoblastic differentiation. We conclude that miR-210 acts as a positive regulator of osteoblastic differentiation by inhibiting the TGF-β/activin signaling pathway through inhibition of AcvR1b.
ISSN:0014-5793
1873-3468
DOI:10.1016/j.febslet.2009.06.006