한빛사논문
- 조회380
Hyun-Kyung So 1,2†, Hyebeen Kim 1,2†, Jinwoo Lee 1,3†, Chang-Lim You 1,2, Chae-Eun Yun 1,2, Hyeon-Ju Jeong 1,2, Eun-Ju Jin 1, Yunju Jo 1, Dongryeol Ryu 1*, Gyu-Un Bae 4*, Jong-Sun Kang 1,2*
1Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon, Korea.
2Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon, Korea.
3Research Institute of Aging-Related Diseases, AniMusCure, Inc., Suwon, Korea.
4Drug Information Research Institute, Muscle Physiome Research Center, College of Pharmacy, Sookmyung Women's University, Seoul, Korea.
*Address correspondence to: J.-S.K.; G.-U.B.; D.R.
†These authors contributed equally to this work.
Abstract
Neuromuscular dysfunction is tightly associated with muscle wasting that occurs with age or due to degenerative diseases. However, the molecular mechanisms underlying neuromuscular dysfunction are currently unclear. Recent studies have proposed important roles of Protein arginine methyltransferase 1 (Prmt1) in muscle stem cell function and muscle maintenance. In the current study, we set out to determine the role of Prmt1 in neuromuscular function by generating mice with motor neuron-specific ablation of Prmt1 (mnKO) using Hb9-Cre. mnKO exhibited age-related motor neuron degeneration and neuromuscular dysfunction leading to premature muscle loss and lethality. Prmt1 deficiency also impaired motor function recovery and muscle reinnervation after sciatic nerve injury. The transcriptome analysis of aged mnKO lumbar spinal cords revealed alterations in genes related to inflammation, cell death, oxidative stress, and mitochondria. Consistently, mnKO lumbar spinal cords of sciatic nerve injury model or aged mice exhibited elevated cellular stress response in motor neurons. Furthermore, Prmt1 inhibition in motor neurons elicited mitochondrial dysfunction. Our findings demonstrate that Prmt1 ablation in motor neurons causes age-related motor neuron degeneration attributing to muscle loss. Thus, Prmt1 is a potential target for the prevention or intervention of sarcopenia and neuromuscular dysfunction related to aging.
논문정보
- Research article
- 2023년 06월 (BRIC 등록일 2023-07-07)
- 국내 연구진
- 의약학 > 분자세포의학
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