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Protein arginine N-methyltransferase 4 (PRMT4) contributes to lymphopenia in experimental sepsis
Journal article   Peer reviewed

Protein arginine N-methyltransferase 4 (PRMT4) contributes to lymphopenia in experimental sepsis

Yandong Lai, Xiuying Li, Tiao Li, Xiaoyun Li, Toru Nyunoya, Kong Chen, Georgios Kitsios, Mehdi Nouraie, Yingze Zhang, Bryan J McVerry, …
Thorax, Vol.78(4), pp.383-393
04/01/2023
DOI: 10.1136/thoraxjnl-2021-217526
PMID: 35354645
url
https://doi.org/10.1136/thoraxjnl-2021-217526View
Published (Version of record) Open Access

Abstract

BackgroundOne hallmark of sepsis is the reduced number of lymphocytes, termed lymphopenia, that occurs from decreased lymphocyte proliferation or increased cell death contributing to immune suppression. Histone modification enzymes regulate immunity by their epigenetic and non-epigenetic functions; however, the role of these enzymes in lymphopenia remains elusive.MethodsWe used molecular biological approaches to investigate the high expression and function of a chromatin modulator protein arginine N-methyltransferase 4 (PRMT4)/coactivator-associated arginine methyltransferase 1 in human samples from septic patients and cellular and animal septic models.ResultsWe identified that PRMT4 is elevated systemically in septic patients and experimental sepsis. Gram-negative bacteria and their derived endotoxin lipopolysaccharide (LPS) increased PRMT4 in B and T lymphocytes and THP-1 monocytes. Single-cell RNA sequencing results indicate an increase of PRMT4 gene expression in activated T lymphocytes. Augmented PRMT4 is crucial for inducing lymphocyte apoptosis but not monocyte THP-1 cells. Ectopic expression of PRMT4 protein caused substantial lymphocyte death via caspase 3-mediated cell death signalling, and knockout of PRMT4 abolished LPS-mediated lymphocyte death. PRMT4 inhibition with a small molecule compound attenuated lymphocyte death in complementary models of sepsis.ConclusionsThese findings demonstrate a previously uncharacterised role of a key chromatin modulator in lymphocyte survival that may shed light on devising therapeutic modalities to lessen the severity of septic immunosuppression.
ARDS Bacterial Infection Lymphocyte Biology Pneumonia Respiratory infection

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