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. 2021 Sep 3;12(9):828. doi: 10.1038/s41419-021-04115-7

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — A–D PRMT4 was silenced or overexpressed by i.t. administered lentiviral constructs for 14 days. Mice were then given (i.t.) LPS with or without a PRMT4 inhibitor as indicated for 24 h (n = 8). Lung tissues were stained with hematoxylin–eosin (H&E) (A, upper panels) and TUNEL staining (A, lower panels). B TUNEL-positive cells in lung tissues were quantitated. C PRMT4 overexpression and knockdown in lung tissues from A were analyzed by immunoblotting. The data from C were quantitated and plotted in D (n = 3). *P < 0.05 vs. scrambled control. Scale bar = 100 μm.