Downregulation of IRS2 in myelodysplastic syndrome: A possible role in impaired hematopoietic cell differentiation

Downregulation of IRS2 in myelodysplastic syndrome: A possible role in impaired hematopoietic cell differentiation

Author Machado-Neto, Joao Agostinho Google Scholar
Favaro, Patricia Autor UNIFESP Google Scholar
Lazarini, Mariana Google Scholar
Santos Duarte, Adriana da Silva Google Scholar
Archangelo, Leticia Froehlich Google Scholar
Lorand-Metze, Irene Google Scholar
Costa, Fernando Ferreira Google Scholar
Olalla Saad, Sara Teresinha Google Scholar
Traina, Fabiola Google Scholar
Institution Universidade Federal de São Paulo (UNIFESP)
Universidade Estadual de Campinas (UNICAMP)
Abstract Insulin receptor substrate 2 (IRS2) is an adaptor protein that associates with the receptor of erythropoietin, insulin-like growth factor 1 and thrombopoietin; however, its role is not known in myelodysplasia. We, herein, report a significantly lower IRS2 expression in MDS cells, compared to normal cells. IRS2 expression was reduced in high-risk, compared to low-risk disease, and positively correlated with neutrophil and platelet counts. IRS2 was upregulated during erythroid differentiation of CD34(+) cells from normal donors and low-risk MDS patients and also during erythroid, granulocytic and megakaryocytic differentiation in cell lines. These results suggest that defective IRS2 expression plays a role in the impaired hematopoietic cell differentiation in MDS. (C) 2012 Elsevier B.V. All rights reserved.
Keywords IRS2
Myelodysplastic syndromes
Erythropoietin
Insulin-like growth factor 1
Differentiation
Language English
Sponsor Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Date 2012-07-01
Published in Leukemia Research. Oxford: Pergamon-Elsevier B.V., v. 36, n. 7, p. 931-935, 2012.
ISSN 0145-2126 (Sherpa/Romeo, impact factor)
Publisher Elsevier B.V.
Extent 931-935
Origin http://dx.doi.org/10.1016/j.leukres.2012.03.002
Access rights Closed access
Type Article
Web of Science ID WOS:000304353400034
URI http://repositorio.unifesp.br/handle/11600/35062

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