UBE2L3, a Partner of MuRF1/TRIM63, Is Involved in the Degradation of Myofibrillar Actin and Myosin

Peris-Moreno, Dulce; Malige, Mélodie; Claustre, Agnès; Armani, Andrea M.; Coudy-Gandilhon, Cécile; Deval, Christiane; Béchet, Daniel; Fafournoux, Pierre; Sandri, Marco; Combaret, Lydie; Taillandier, Daniel; Polge, Cécile

doi:10.3390/cells10081974

Cited by 13 publications

(10 citation statements)

References 63 publications

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“…Atrogin-1 and MuRF-1 were two key musclespecific E3 ubiquitin ligases regarded as the markers of muscle atrophy, and also proved to be related to the mechanisms of BJD improving muscle atrophy in cancer cachexia (Bodine and Baehr, 2014;Zhang et al, 2017;Zhang et al, 2018;Wang et al, 2020). Studies have shown that atrogin-1 and MuRF-1 targeted several myofibrillar proteins for degradation, including a-actin within the ubiquitin-proteasome system (Peris-Moreno et al, 2021). Considering that we have previously proved that BJD treatment inhibited the protein expressions of atrogin-1 and MuRF-1 in Apc Min/+ mice (Supplementary Figure S2), we detected the protein expression of a-actin and MyoD in this study (Figures 2E,F).…”

Section: Discussionmentioning

confidence: 99%

Baoyuan Jiedu decoction alleviating cancer cachexia–Induced muscle atrophy by regulating muscle mitochondrial function in ApcMin/+ mice

Zhang

Huang

et al. 2022

Front. Pharmacol.

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Cancer cachexia is a complex syndrome that leads to an ongoing loss of skeletal muscle mass in many malignant tumors. Our previous studies have evaluated the effectiveness of Baoyuan Jiedu decoction (BJD) in alleviating cancer-induced muscle atrophy. However, the mechanisms of BJD regulating muscle atrophy could not be fully understood. Therefore, we further investigated the mechanisms of BJD mitigating muscle atrophy both in an ApcMin/+ mouse model and the Lewis-conditioned medium–induced C2C12 myotube atrophy model. We confirmed the quality of BJD extracts by HPLC. In an In vivo study, body weight loss and muscle atrophy were alleviated with BJD treatment. GO analysis suggested that ATP metabolism and mitochondria were involved. The results of the electron microscope show that BJD treatment may have a healing effect on mitochondrial structure. Moreover, ATP content and mitochondrial numbers were improved with BJD treatment. Furthermore, both in vivo and in vitro, we demonstrated that the BJD treatment could improve mitochondrial function owing to the increased number of mitochondria, balanced dynamic, and regulation of the electron transport chain according to the protein and mRNA expressions. In addition, oxidative stress caused by mitochondrial dysfunction was ameliorated by BJD treatment in ApcMin/+ mice. Consequently, our study provides proof for BJD treatment alleviating cancer cachexia–induced muscle atrophy by modulating mitochondrial function in ApcMin/+ mice.

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Section: Discussionmentioning

confidence: 99%

Baoyuan Jiedu decoction alleviating cancer cachexia–Induced muscle atrophy by regulating muscle mitochondrial function in ApcMin/+ mice

Zhang

Huang

et al. 2022

Front. Pharmacol.

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“…PI3K/AKT/mTOR signalling pathway silencing and aging-induced inflammation can activate the UPS, which decreases contractile proteins and increases the average distance between MyHC and F-actin. 57 Muscle fibre atrophy and reductions in muscle fibre-specific force and unloaded shortening velocity are widely recognized as significant contributors to the development of sarcopenia. 8 Under energy stress, AMPK phosphorylates FoxO3 Ser413/588 and activates it.…”

Section: Ubiquitinationmentioning

confidence: 99%

Post‐translational regulation of muscle growth, muscle aging and sarcopenia

Zhong

Zheng

et al. 2023

J cachexia sarcopenia muscle

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Skeletal muscle makes up 30-40% of the total body mass. It is of great significance in maintaining digestion, inhaling and exhaling, sustaining body posture, exercising, protecting joints and many other aspects. Moreover, muscle is also an important metabolic organ that helps to maintain the balance of sugar and fat. Defective skeletal muscle function not only limits the daily activities of the elderly but also increases the risk of disability, hospitalization and death, placing a huge burden on society and the healthcare system. Sarcopenia is a progressive decline in muscle mass, muscle strength and muscle function with age caused by environmental and genetic factors, such as the abnormal regulation of protein post-translational modifications (PTMs).

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“…MuRF1 can targets for degradation several myofibrillar proteins, and UBE2L3 exhibited a high affinity for MuRF1. 18,19 Intermittent exercise can reduce the expression of MuRF1 by inhibiting NF-κB to improve the degradation of skeletal muscle protein. Similarly, endurance training can also inhibit the activation of NF-κB, thereby reducing the expression of MAFbx and MuRF1, and reducing the occurrence of skeletal muscle atrophy.…”

Section: Nf-κb / Murf1 Pathway and Mechanisms Of Muscle Atrophymentioning

confidence: 99%

Effects of Contusion and Exhaustive Exercise on Murf1 and Mafbx in the Skeletal Muscle of Rats

Tong-bin

Wang

et al. 2023

Rev Bras Med Esporte

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Objective To study the effects of contusion and exhaustive exercise on the expression of degradation-related factors MuRF1 and MAFbx in the skeletal muscle of rats and describe the repair mechanism of skeletal muscle injury. Methods Forty-two male SD rats were randomly divided into 7 groups. The rats in each group were killed at different time points (0h, 24h, 48h) after exhaustive exercise (E0, E24, E48) and contusion (D0, D24, D48), respectively, and in the resting state in control group (C). The right gastrocnemius muscles were resected and divided into two parts, one for the mRNAs of MuRF1 and MAFbx by real-time PCR, and the other for protein measurement by Western blotting. Results Compared with the control group, the MuRF1 mRNA and protein expression of the skeletal muscle in the E0 group was markedly increased (P <0.05) and followed by a downward trend in E24 the E48 groups. On the other hand, MuRF1 mRNA expression of the skeletal muscle in the D24 group was significantly upregulated (P <0.01), then decreased in the D48 group (P <0.01). Meanwhile, compared with the C group, MAFbx mRNA gene expression continued to be upregulated in D24 and D48 (P <0.05), but decreased in E24 and E48 (p<0.01). On the other hand, the NF-κB protein contents of the skeletal muscle in the D0, D24, and D48 groups, as well as in the E48 group, were markedly downregulated (P <0.05), and the one in E48 was also remarkably downregulated (P <0.05). Conclusion NF-κB may negatively regulate the process of protein degradation by the NF-κB / MuRF1 signal pathway. Level of evidence III; Therapeutic studies investigating the results of treatment.

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UBE2L3, a Partner of MuRF1/TRIM63, Is Involved in the Degradation of Myofibrillar Actin and Myosin

Cited by 13 publications

References 63 publications

Baoyuan Jiedu decoction alleviating cancer cachexia–Induced muscle atrophy by regulating muscle mitochondrial function in ApcMin/+ mice

Baoyuan Jiedu decoction alleviating cancer cachexia–Induced muscle atrophy by regulating muscle mitochondrial function in ApcMin/+ mice

Post‐translational regulation of muscle growth, muscle aging and sarcopenia

Effects of Contusion and Exhaustive Exercise on Murf1 and Mafbx in the Skeletal Muscle of Rats

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