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Progranulin facilitates the increase of platelet count in immune thrombocytopenia.

Authors
  • Yu, Yingyi1
  • Shi, Yuanyuan2
  • Zuo, Xinyi1
  • Feng, Qi1
  • Hou, Yu1
  • Tang, Wei2
  • Lu, Yi3
  • Yi, Fan4
  • Hou, Ming1
  • Yu, Yuan5
  • Peng, Jun6
  • 1 Department of Hematology, Qilu Hospital, Shandong University, Jinan, China. , (China)
  • 2 Department of Pathogenic Biology, Shandong University School of Basic Medical Sciences, China. , (China)
  • 3 Department of Biochemistry and Molecular Biology, Shandong University School of Basic Medical Sciences, China. , (China)
  • 4 Department of Pharmacology, Shandong University School of Medicine, Jinan, China. , (China)
  • 5 Department of Hematology, Qilu Hospital, Shandong University, Jinan, China; Shandong Provincial Key Laboratory of Immunohematology, Qilu Hospital, Shandong University, Jinan, China. Electronic address: [email protected] , (China)
  • 6 Department of Hematology, Qilu Hospital, Shandong University, Jinan, China. Electronic address: [email protected] , (China)
Type
Published Article
Journal
Thrombosis research
Publication Date
Apr 01, 2018
Volume
164
Pages
24–31
Identifiers
DOI: 10.1016/j.thromres.2018.02.137
PMID: 29475178
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Progranulin (PGRN) is emerging as a critical immune mediator involved in a variety of autoimmune disorders. However, its role in immune thrombocytopenia (ITP) remains unclear. In this study, the enzyme-linked immunosorbent assay was used for determining the plasma levels of PGRN in ITP patients vs. healthy controls. In addition, the role of PGRN in ITP was investigated in two kinds of ITP murine models. Further, we explored whether PGRN functioned by affecting the number of T regulatory cells (Tregs) using flow cytometry. We first observed that plasma levels of PGRN were significantly elevated in ITP patients (n = 52) compared to healthy controls (n = 40), and the levels of PGRN declined in patients after receiving treatment. Additionally, we found a negative correlation between plasma PGRN levels and platelet count of ITP patients, suggesting that PGRN is involved in the pathogenesis of ITP. PGRN deficiency further decreased platelet count in a passive-transfer ITP murine model. By contrast, administration of recombinant PGRN increased platelet count in SCID mice with chronic ITP. Meanwhile, PGRN deficiency impaired proliferation of Tregs in the passive transfer ITP murine model. These data suggest that PGRN may exert a protective role in ITP by promoting Treg proliferation. Our study revealed a new regulator involved in the pathogenesis of ITP and provided a potential strategy for management of ITP. Copyright © 2018. Published by Elsevier Ltd.

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