Please use this identifier to cite or link to this item: https://hdl.handle.net/10356/88100
Title: Alternative splicing analysis in human monocytes and macrophages reveals MBNL1 as major regulator
Authors: Lorenzini, Paolo A.
Wong, Mei Su M.
Liu, Hongfei
Zhang, Fan
Xu, Shaohai
Zheng, Jie
Roca, Xavier
Keywords: DRNTU::Science::Biological sciences
Alternative Splicing
Human Monocytes
Issue Date: 2018
Source: Liu, H., Lorenzini, P. A., Zhang, F., Xu, S., Wong, M. S. M., Zheng, J., et al. (2018). Alternative splicing analysis in human monocytes and macrophages reveals MBNL1 as major regulator. Nucleic Acids Research, 46(12), 6069-6086.
Series/Report no.: Nucleic Acids Research
Abstract: We report the detailed transcriptomic profiles of human innate myeloid cells using RNA sequencing. Monocytes migrate from blood into infected or wounded tissue to differentiate into macrophages, and control inflammation via phagocytosis or cytokine secretion. We differentiated culture primary monocytes with either GM- or M-CSF to obtain pro- or anti-inflammatory macrophages, and respectively activated them with either LPS/IFNγ or anti-inflammatory cytokines. We also treated the THP-1 monocytic cell line with PMA and similar cytokines to mimic differentiation and activation. We detected thousands of expression and alternative-splicing changes during monocyte-to-macrophage differentiation and activation, and a net increase in exon inclusion. MBNL1 knockdown phenocopies several alternative-splicing changes and strongly impairs PMA differentiation, suggesting functional defects in monocytes from Myotonic Dystrophy patients. This study provides general insights into alternative splicing in the monocyte–macrophage lineage, whose future characterization will elucidate their contribution to immune functions, which are altered in immunodeficiencies, autoimmunity, atherosclerosis and cancer.
URI: https://hdl.handle.net/10356/88100
http://hdl.handle.net/10220/45607
ISSN: 0305-1048
DOI: 10.1093/nar/gky401
Rights: © 2018 The Author(s). Published by Oxford University Press on behalf of Nucleic Acids Research. This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
Fulltext Permission: open
Fulltext Availability: With Fulltext
Appears in Collections:SBS Journal Articles

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