albumin - publications

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1. Blood. 2012 Feb 6. [Epub ahead of print]

Downregulated expression of hsa-miR-181c in Fanconi anemia patients: implications
in TNFα regulation and proliferation of hematopoietic progenitor cells.

Río P, Agirre X, Garate L, Baños R, Alvarez L, San José-Enériz E, Badell I,
Casado JA, Garín M, Prósper F, Bueren JA.

Hematopoiesis & Gene Therapy, Centro de Investigaciones Energeticas,
Medioambientales y Tecnologicas, and Centro de Investigacion Biomedica en Red de
Enfermedades Raras, Madrid, Spain;

Fanconi anemia (FA) is an inherited genetic disorder associated with BM failure
and cancer predisposition. In this study we aimed to elucidate the role of miRNAs
in the hematopoietic defects observed in FA patients. Initial studies showed that
three miRNAs, hsa-miR-133a, hsa-miR-135b and hsa-miR-181c were significantly
down-regulated in lymphoblastoid cell lines and fresh peripheral blood cells from
FA patients. In vitro studies with cells expressing the luciferase reporter fused
to the TNFα 3'UTR confirmed in silico predictions suggesting the interaction of
hsa-miR-181c with TNFα mRNA. These observations were consistent with the
downregulated expression of TNFα mediated by hsa-miR-181c in cells from healthy
donors and FA patients. Because of the relevance of TNFα in the hematopoietic
defects of FA patients, BM cells from FA patients were transfected with
hsa-miR-181c to evaluate the impact of this miRNA in their clonogenic potential.
Strikingly we observed that hsa-miR-181c markedly increased the number and size
of the myeloid and erythroid colonies generated by FA BM cells. Taken together
our results offer new clues to understand the biological basis of the BM failure
in FA patients, and open new perspectives for the treatment of the hematological
dysfunction in FA patients based on miRNA regulation.

PMID: 22310912 [PubMed - as supplied by publisher]