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泛素-蛋白酶体系统在CCL5/RANTES诱导的类肌肉减少症表型中的作用

Role of the ubiquitin-proteasome system in the sarcopenic-like phenotype induced by CCL5/RANTES.

作者信息

Conejeros-Lillo Sabrina, Aguirre Francisco, Cabrera Daniel, Simon Felipe, Peñailillo Luis, Cabello-Verrugio Claudio

机构信息

Laboratory of Muscle Pathology, Fragility and Aging, Department of Biological Sciences, Faculty of Life Sciences, Universidad Andres Bello, Santiago, Chile; Millennium Institute on Immunology and Immunotherapy, Faculty of Life Sciences, Universidad Andres Bello, Santiago.

Departamento de Gastroenterología, Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile; Facultad de Ciencias Médicas, Escuela de Medicina, Universidad Bernardo O Higgins, Santiago.

出版信息

Eur J Transl Myol. 2024 Feb 15;34(1):12249. doi: 10.4081/ejtm.2024.12249.

DOI:10.4081/ejtm.2024.12249
PMID:38357936
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11017164/
Abstract

Sarcopenia is characterized by reduced muscle strength and mass and a decline in muscle fiber diameter and amount of sarcomeric proteins. Sarcopenia involves the activation of the ubiquitin-proteasome system (UPS). MuRF-1 and atrogin-1 are E3 ubiquitin ligases belonging to UPS, leading to proteolysis mediated by the PSMB 5, 6, and 7 subunits of 20S proteasome. CCL5/RANTES induces a sarcopenic-like effect in muscle cells. The present work explored the impact of CCL5 on UPS components and the influence of UPS on its sarcopenic-like effect. We demonstrated that CCL5 increased MuRF-1 and atrogin-1 protein levels and mRNA levels of subunits PSMB 5, 6, and 7. We used the MG132 inhibitor to elucidate the role of the 20S proteasome in the CCL5-induced sarcopenic-like effect. This inhibitor prevented the decrease in troponin and MHC protein levels and partially prevented the reduction in the diameter of single-isolated FDB muscle fibers induced by CCL5. These findings indicate that CCL5 actively modulates the UPS. Moreover, our results show the direct participation of UPS in the sarcopenic-like phenotype induced by CCL5.

摘要

肌肉减少症的特征是肌肉力量和质量下降，肌纤维直径和肌节蛋白数量减少。肌肉减少症涉及泛素 - 蛋白酶体系统（UPS）的激活。MuRF - 1和atrogin - 1是属于UPS的E3泛素连接酶，导致由20S蛋白酶体的PSMB 5、6和7亚基介导的蛋白水解。CCL5/RANTES在肌肉细胞中诱导类似肌肉减少症的效应。本研究探讨了CCL5对UPS成分的影响以及UPS对其类似肌肉减少症效应的影响。我们证明CCL5增加了MuRF - 1和atrogin - 1蛋白水平以及PSMB 5、6和7亚基的mRNA水平。我们使用MG132抑制剂来阐明20S蛋白酶体在CCL5诱导的类似肌肉减少症效应中的作用。该抑制剂阻止了肌钙蛋白和MHC蛋白水平的降低，并部分阻止了CCL5诱导的单根分离FDB肌纤维直径的减小。这些发现表明CCL5积极调节UPS。此外，我们的结果表明UPS直接参与了CCL5诱导的类似肌肉减少症的表型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/912faac38ff7/ejtm-34-1-12249-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/dc22192b5c5c/ejtm-34-1-12249-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/ac08548f8a18/ejtm-34-1-12249-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/7bf8c8b88b40/ejtm-34-1-12249-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/912faac38ff7/ejtm-34-1-12249-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/dc22192b5c5c/ejtm-34-1-12249-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/ac08548f8a18/ejtm-34-1-12249-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/7bf8c8b88b40/ejtm-34-1-12249-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/29a9/11017164/912faac38ff7/ejtm-34-1-12249-g004.jpg

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