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PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation

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Abstract

Angiotensin II (AngII) has potent cardiac hypertrophic effects mediated through activation of hypertrophic signaling like Wnt/β-Catenin signaling. In the current study, we examined the role of protein arginine methyltransferase 7 (PRMT7) in cardiac function. PRMT7 was greatly decreased in hypertrophic hearts chronically infused with AngII and cardiomyocytes treated with AngII. PRMT7 depletion in rat cardiomyocytes resulted in hypertrophic responses. Consistently, mice lacking PRMT7 exhibited the cardiac hypertrophy and fibrosis. PRMT7 overexpression abrogated the cellular hypertrophy elicited by AngII, while PRMT7 depletion exacerbated the hypertrophic response caused by AngII. Similar with AngII treatment, the cardiac transcriptome analysis of PRMT7-deficient hearts revealed the alteration in gene expression profile related to Wnt signaling pathway. Inhibition of PRMT7 by gene deletion or an inhibitor treatment enhanced the activity of β-catenin. PRMT7 deficiency decreases symmetric dimethylation of β-catenin. Mechanistic studies reveal that methylation of arginine residue 93 in β-catenin decreases the activity of β-catenin. Taken together, our data suggest that PRMT7 is important for normal cardiac function through suppression of β-catenin activity.

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All data related to this work is presented in the paper and its supplements. The materials used in this study are available to any qualified researcher upon reasonable request addressed to J.S.K.

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Acknowledgements

This research was supported by the National Research Foundation Grant funded by the Korean Government (MSIP) (NRF-2019R1A2C2006233; NRF-2017M3A9D8048710; 2016R1A5A2945889).

Funding

This research received no external funding.

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Author notes

  1. Byeong-Yun Ahn, Myong-Ho Jeong have contributed equally to this work.

Authors and Affiliations

  1. Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, 2066, Seobu-Ro, Jangan-gu, Suwon, 16419, Gyeonggi-do, Republic of Korea

    Byeong-Yun Ahn, Myong-Ho Jeong, Jung-Hoon Pyun, Hyeon-Ju Jeong, Tuan Anh Vuong, Ju-Hyeon Bae, Subin An, Su Woo Kim, Dongryeol Ryu & Jong-Sun Kang

  2. Department of Physiology, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea

    Hyun-Ji Kim & Hana Cho

  3. Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, Republic of Korea

    Byeong-Yun Ahn, Myong-Ho Jeong, Jung-Hoon Pyun, Hyeon-Ju Jeong, Tuan Anh Vuong, Ju-Hyeon Bae, Subin An, Su Woo Kim, Hyun-Ji Kim, Hana Cho & Jong-Sun Kang

  4. Division of Cardiovascular Diseases, Center for Biomedical Sciences, National Institute of Health, Cheongju, Chungbuk, Republic of Korea

    Myong-Ho Jeong

  5. Research Institute of Aging-Related Disease, AniMusCure, Inc., Suwon, Republic of Korea

    Tuan Anh Vuong

  6. Drug Information Research Institute, College of Pharmacy, Sookmyung Women’s University, 100 Cheongpa-ro 47-gil, Seoul, 04310, Republic of Korea

    Yong Kee Kim & Gyu-Un Bae

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Contributions

BYA, MHJ, JHP, HJJ, TAV, JHB, SA, SWK, YKK, DR, HJK, HC, GUB, and JSK contributed to the experimental design, research and data analysis. BYA, MHJ, GUB, and JSK wrote the manuscript.

Corresponding authors

Correspondence to Gyu-Un Bae or Jong-Sun Kang.

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The authors have declared that no conflict of interest exists.

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All experimental protocols were approved by the Institutional Animal Care for Ethics and Use Committee of Sunkyunkwan University (SUSM, SKKUIACUC 2018-11-14-2), and the study followed institutional and National Institutes of Health guidelines for laboratory animal care.

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18_2021_4097_MOESM1_ESM.pdf

Fig. S1. PRMT7 expression in hearts and cardiomyocytes. (a) Immunohistochemistry for PRMT7 in normal human left atrial appendage. Rabbit IgG was used as isotype control. Scale bar: 100 µm. (b) Representative images for immunostaining of PRMT7 in mouse heart tissue. CX43 (red): gap junction protein Connexin 43 for the formation of heart structures. DAPI (4′,6-diamidino-2-phenylindole): blue-fluorescent DNA stain. Scale bar: 20 µm. (c) Representative images for immunostaining of PRMT7 in neonatal rat ventricular cardiomyocytes (NRVMs). Scale bar: 10 µm

18_2021_4097_MOESM2_ESM.pdf

Fig. S2. PRMT7 deletion induces cardiomyocyte hypertrophy. (a) The capacitance of NRVM cells transfected with control or shPRMT7. n=3, *p<0.05. Data represent mean ±SEM. (b) Representative images for isolated primary cardiomyocytes from WT and KO heart. Scale bar: 100 μm. Arrow= cardiomyocytes, Asterisk= non-cardiomyocytes. (c) Quantification of cell surface area in panel b. *p<0.05, #p<0.005, NS: not significant, n=143 for WT, n=73 for KO. Data represent mean ±SEM. (d) Physiological analysis for cellular capacitances isolated atrial (left) and ventricular (right) myocytes in WT and KO. **p<0.01. Data represent mean ±SD

18_2021_4097_MOESM3_ESM.pdf

Fig. S3. A negative correlation between PRMT7 and β-Catenin. (a) A schematic illustration demonstrating the stepwise workflow of a transcriptome analysis: collect the gene expression profile for hearts, normalize the value of gene expression to Z-score, and analyze the correlation between PRMT7 and potential target genes. (b) The scatter plots presenting the correlated expression patterns between PRMT7 (X-axis) and the target genes; Ctnnb1, Axin2, Gsk3b, and Isl1 (Y-axis). (c) The scatter plot presenting the correlated expression patterns between PRMT7 (X-axis) and Ctnnb1 (Y-axis) in 4 organisms; Homo sapiens, Mus musculus, Canis lupus, and Danio rerio

18_2021_4097_MOESM4_ESM.pdf

Fig. S4. Symmetric arginine di-methylation of β-Catenin is regulated likely by PRMT7. In vitro methylation analysis of recombinant GST-tagged β-Catenin in the presence SAM and purified HA-PRMT7 (P7) and HA-tagged inactive form of PMRT7 (iP7) by immunoprecipitation. The methylation status was detected by immunoblotting with anti-MMA and anti-Sym10 antibodies

18_2021_4097_MOESM5_ESM.pdf

Fig. S5. Working hypothesis. PRMT7 modulates the level of β-Catenin via methylation at arginine 93 in cardiomyocytes. PRMT7 deficiency in cardiomyocytes causes elevated β-Catenin activities, leading to cardiac hypertrophy and fibrosis. Illustration was created with BioRender

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Ahn, BY., Jeong, MH., Pyun, JH. et al. PRMT7 ablation in cardiomyocytes causes cardiac hypertrophy and fibrosis through β-catenin dysregulation. Cell. Mol. Life Sci. 79, 99 (2022). https://doi.org/10.1007/s00018-021-04097-x

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