| pubmed-article:19342382 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19342382 | lifeskim:mentions | umls-concept:C0277784 | lld:lifeskim |
| pubmed-article:19342382 | lifeskim:mentions | umls-concept:C1159977 | lld:lifeskim |
| pubmed-article:19342382 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:19342382 | pubmed:issue | 23 | lld:pubmed |
| pubmed-article:19342382 | pubmed:dateCreated | 2009-6-1 | lld:pubmed |
| pubmed-article:19342382 | pubmed:abstractText | Bone tissue arises from mesenchymal cells induced into the osteoblast lineage by essential transcription factors and signaling cascades. MicroRNAs regulate biological processes by binding to mRNA 3'-untranslated region (UTR) sequences to attenuate protein synthesis. Here we performed microRNA profiling and identified miRs that are up-regulated through stages of osteoblast differentiation. Among these are the miR-29, miR-let-7, and miR-26 families that target many collagens and extracellular matrix proteins. We find that miR-29b supports osteoblast differentiation through several mechanisms. miR-29b decreased and anti-miR-29b increased activity of COL1A1, COL5A3, and COL4A2 3'-UTR sequences in reporter assays, as well as endogenous gene expression. These results support a mechanism for regulating collagen protein accumulation during the mineralization stage when miR-29b reaches peak levels. We propose that this mechanism prevents fibrosis and facilitates mineral deposition. Our studies further demonstrate that miR-29b promotes osteogenesis by directly down-regulating known inhibitors of osteoblast differentiation, HDAC4, TGFbeta3, ACVR2A, CTNNBIP1, and DUSP2 proteins through binding to target 3'-UTR sequences in their mRNAs. Thus, miR-29b is a key regulator of development of the osteoblast phenotype by targeting anti-osteogenic factors and modulating bone extracellular matrix proteins. | lld:pubmed |
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| pubmed-article:19342382 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19342382 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19342382 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:19342382 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19342382 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19342382 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:19342382 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:SteinGary SGS | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:SteinJanet... | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:LianJane BJB | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:van... | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:GarzonRamiroR | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:CroceCarlo... | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:HassanMohamma... | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:AqeilanRami... | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:LiZhaoyongZ | lld:pubmed |
| pubmed-article:19342382 | pubmed:author | pubmed-author:JafferjiMoham... | lld:pubmed |
| pubmed-article:19342382 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:19342382 | pubmed:day | 5 | lld:pubmed |
