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Aberrant expression of Notch signaling molecules in patients with immune thrombocytopenic purpura

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Abstract

To investigate the role of Notch signaling pathway in immune thrombocytopenic purpura (ITP), we measured the expression of 11 Notch pathway molecules in ITP patients and evaluated their clinical relevance. Real-time reverse transcriptase polymerase chain reaction results showed there was aberrant expression of some Notch molecules in ITP. Notch1 and Notch3 expression elevated, while Notch2 decreased statistically in ITP patients. As for Notch ligands, only DLL1 was found downregulated in ITP. The expression of Notch target gene, Hes1, was also upregulated. In accordance with the mRNA level, Notch1 and Hes1 protein expression was also found elevated by Western blot. Immunocytochemistry showed that Notch1 expressed highly in the cytomembrane, cytoplasm, and part of cellular nucleus for ITP while weak in cytomembrane for controls, and Hes1 of ITP was found expressed higher in cellular nucleus than that of controls. Our findings suggest that the aberrant expression profile of Notch pathway may be involved in ITP, and blockage of Notch1 pathway is likely a promising therapeutic concept.

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Acknowledgments

This study was partially supported by grants from the National Natural Science Foundation (30600680, 30471941, 30770922, 30470742, 30570779, 30600259, 30628015 and 30300312), 973 Project (2006CB503800), Key Clinical Research Project of Chinese Ministry of Health (2007–2009), Research Project of National Public Fare (200802031), and the Shandong Technological Development Project (2005BS03022, 2005GG4202018 and Q2008C07), and Taishan Scholar Fundation.

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Correspondence to Daoxin Ma.

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Jianjian Dai and Xiaojuan Zhu contributed equally to this work.

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Supplementary Material: Results (22 ITP and 22 controls) (XLS 31 kb)

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Ma, D., Dai, J., Zhu, X. et al. Aberrant expression of Notch signaling molecules in patients with immune thrombocytopenic purpura. Ann Hematol 89, 155–161 (2010). https://doi.org/10.1007/s00277-009-0790-y

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  • DOI: https://doi.org/10.1007/s00277-009-0790-y

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