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J Leukoc Biol. 2017 May;101(5):1109-1117. doi: 10.1189/jlb.1RU0916-391RR. Epub 2017 Feb 24.

Development of platelets during steady state and inflammation.

Author information

1
Institute of Biochemistry and Molecular Biology, RWTH Aachen University, Aachen, Germany.
2
Department of Urology, University Medicine, Greifswald, Germany.
3
Institute for Occupational and Social Medicine, RWTH Aachen University, Aachen, Germany.
4
Institute for Occupational and Social Medicine, RWTH Aachen University, Aachen, Germany pziegler@ukaachen.de.

Abstract

Megakaryocytes (MK) are the sole source of platelets in the body. They develop from lineage-committed hematopoietic stem and progenitor cells (HSPCs) via intermediate cells, which differ in morphology, size, ploidy, and surface phenotype. Development and maturation of MKs is governed by different transcription factors, including GATA-1, E26 transformation-specific transcription factor (ETS) family members, nuclear factor erythroid 2 transcription factor (NF-E2), and STAT3. During such challenges as acute inflammation, platelets are consumed in high numbers and must be replenished to secure survival of the host. This is achieved by integration of inflammatory signals into early MK development and depends on the STAT1-mediated enhanced translation of transcripts in stem cell-like megakaryocyte progenitors. Here, we review recent developments, which highlight the impact of inflammation on the development of platelets from HSPCs.

KEYWORDS:

emergency megakaryopoiesis; hematopoietic progenitor cells; interferon

PMID:
28235774
DOI:
10.1189/jlb.1RU0916-391RR
[Indexed for MEDLINE]

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