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. 2025 May 15;39(9):e70579.
doi: 10.1096/fj.202403269R.

PRMT1 Upregulates SIRT6 by Enhancing Arginine Methylation of E2F7 to Inhibit Vascular Smooth Muscle Cell Senescence in Aortic Dissection

Yukun Wu  1 , Xiao Qin  2 , Mengxiang Xiang  1 , Jiangbei Deng  1
Affiliations

PRMT1 Upregulates SIRT6 by Enhancing Arginine Methylation of E2F7 to Inhibit Vascular Smooth Muscle Cell Senescence in Aortic Dissection

Yukun Wu et al. FASEB J. .

Abstract

Aortic dissection (AD) is a highly alarming clinical condition of the aorta, with a significant mortality rate. Vascular smooth muscle cell (VSMC) senescence dominantly promotes AD progression. This study planned to clarify the exact functions and mechanisms of protein arginine methyltransferase 1 (PRMT1), E2F7, and Sirtuin 6 (SIRT6) in the VSMC senescence of the AD model. Angiotensin II (Ang II) and β-Aminopropionitrile (BAPN) were used to treat VSMCs or C57BL/6J mice to establish the AD in vitro or in vivo model. Protein expressions were examined by western blot, IHC, and IF staining. Histological change or cell senescence was monitored using H&E or senescence-associated-β-galactosidase (SA-β-gal) staining. Enzyme-Linked Immunosorbent Assay (ELISA) assays were utilized to evaluate senescence-associated secretory phenotype markers' levels. The binding interactions between E2F7 and SIRT6 or PRMT1 and E2F7 were verified by the luciferase reporter, ChIP Co-IP, and GST-pull-down analysis. The ubiquitination levels of E2F7 were assessed using ubiquitination assays. PRMT1, E2F7, and SIRT6 protein levels were decreased in the Ang II-treated VSMCs of the AD model. Moreover, E2F7 repressed cell senescence by transcriptionally regulating SIRT6 in the AD model. PRMT1 silencing promoted cell senescence of VSMCs under Ang II. Further, PRMT1-mediated arginine methylation could maintain the protein stability of E2F7. PRMT1 restrained cell senescence of VSMCs via the E2F7/SIRT6 axis in the AD model. PRMT1 enhanced arginine methylation of E2F7, leading to the upregulation of SIRT6, thereby inhibiting the senescence of VSMCs in the AD model.

Keywords: E2F7; PRMT1; SIRT6; aortic dissection; arginine acetylation.

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References

    1. H. H. Sievers, B. Rylski, M. Czerny, et al., “Aortic Dissection Reconsidered: Type, Entry Site, Malperfusion Classification Adding Clarity and Enabling Outcome Prediction,” Interactive Cardiovascular and Thoracic Surgery 30, no. 3 (2020): 451–457.
    1. T. Carrel, T. M. Sundt, 3rd, Y. von Kodolitsch, and M. Czerny, “Acute Aortic Dissection,” Lancet 401, no. 10378 (2023): 773–788.
    1. Y. Zhu, B. Lingala, M. Baiocchi, et al., “Type A Aortic Dissection‐Experience Over 5 Decades: JACC Historical Breakthroughs in Perspective,” Journal of the American College of Cardiology 76, no. 14 (2020): 1703–1713.
    1. R. O. Tadros, G. H. L. Tang, H. J. Barnes, et al., “Optimal Treatment of Uncomplicated Type B Aortic Dissection: JACC Review Topic of the Week,” Journal of the American College of Cardiology 74, no. 11 (2019): 1494–1504, https://doi.org/10.1016/j.jacc.2019.07.063.
    1. X. Liu, W. Chen, G. Zhu, et al., “Single‐Cell RNA Sequencing Identifies an Il1rn(+)/Trem1(+) Macrophage Subpopulation as a Cellular Target for Mitigating the Progression of Thoracic Aortic Aneurysm and Dissection,” Cell Discovery 8, no. 1 (2022): 11.

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