| pubmed-article:16330772 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16330772 | lifeskim:mentions | umls-concept:C1537859 | lld:lifeskim |
| pubmed-article:16330772 | lifeskim:mentions | umls-concept:C0014819 | lld:lifeskim |
| pubmed-article:16330772 | lifeskim:mentions | umls-concept:C0007595 | lld:lifeskim |
| pubmed-article:16330772 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
| pubmed-article:16330772 | lifeskim:mentions | umls-concept:C0205307 | lld:lifeskim |
| pubmed-article:16330772 | lifeskim:mentions | umls-concept:C1690540 | lld:lifeskim |
| pubmed-article:16330772 | pubmed:issue | 50 | lld:pubmed |
| pubmed-article:16330772 | pubmed:dateCreated | 2005-12-14 | lld:pubmed |
| pubmed-article:16330772 | pubmed:abstractText | MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression primarily through translational repression. In erythropoietic (E) culture of cord blood CD34+ progenitor cells, the level of miR 221 and 222 is gradually and sharply down-modulated. Hypothetically, this decline could promote erythropoiesis by unblocking expression of key functional proteins. Indeed, (i) bioinformatic analysis suggested that miR 221 and 222 target the 3' UTR of kit mRNA; (ii) the luciferase assay confirmed that both miRs directly interact with the kit mRNA target site; and (iii) in E culture undergoing exponential cell growth, miR down-modulation is inversely related to increasing kit protein expression, whereas the kit mRNA level is relatively stable. Functional studies show that treatment of CD34+ progenitors with miR 221 and 222, via oligonucleotide transfection or lentiviral vector infection, causes impaired proliferation and accelerated differentiation of E cells, coupled with down-modulation of kit protein: this phenomenon, observed in E culture releasing endogenous kit ligand, is magnified in E culture supplemented with kit ligand. Furthermore, transplantation experiments in NOD-SCID mice reveal that miR 221 and 222 treatment of CD34+ cells impairs their engraftment capacity and stem cell activity. Finally, miR 221 and 222 gene transfer impairs proliferation of the kit+ TF-1 erythroleukemic cell line. Altogether, our studies indicate that the decline of miR 221 and 222 during exponential E growth unblocks kit protein production at mRNA level, thus leading to expansion of early erythroblasts. Furthermore, the results on kit+ erythroleukemic cells suggest a potential role of these miRs in cancer therapy. | lld:pubmed |
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| pubmed-article:16330772 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:16330772 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16330772 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16330772 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:16330772 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:16330772 | pubmed:author | pubmed-author:LiuChang-Gong... | lld:pubmed |
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| pubmed-article:16330772 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16330772 | pubmed:day | 13 | lld:pubmed |
| pubmed-article:16330772 | pubmed:volume | 102 | lld:pubmed |
| pubmed-article:16330772 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16330772 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16330772 | pubmed:pagination | 18081-6 | lld:pubmed |
| pubmed-article:16330772 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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| pubmed-article:16330772 | pubmed:year | 2005 | lld:pubmed |
| pubmed-article:16330772 | pubmed:articleTitle | MicroRNAs 221 and 222 inhibit normal erythropoiesis and erythroleukemic cell growth via kit receptor down-modulation. | lld:pubmed |
| pubmed-article:16330772 | pubmed:affiliation | Department of Hematology, Oncology, and Molecular Medicine, Istituto Superiore di Sanità, Rome, Italy. | lld:pubmed |
| pubmed-article:16330772 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16330772 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:16330772 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:16330772 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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