Electrical Stimulation Attenuates Disuse Muscular Atrophy by Modulating Endoplasmic Reticulum Stress-induced Parkin-dependent Mitophagy

Abstract Background: The aim of this study was to investigate the therapeutic effect of electrical stimulation on disuse muscular atrophy in a rabbit model of knee joint contracture and explore the role of endoplasmic reticulum stress-induced Parkin-dependent mitophagy in this process.Methods: Two sub-experiments were carried out successively in our study. In the first sub-experiment, 24 rabbits were divided into four groups on average based on the immobilization time: Ctrl 1, I-2, I-4, and I-6 groups. In the second sub-experiment, 24 rabbits were also divided into four groups on average in accordance with the process mode: Ctrl2, ES, NR, and EST groups. To test the time-dependent changes of the rectus femoris muscles after immobilization in rabbits, and to evaluate the effect of electrical stimulation on the atrophic rectus femoris muscles, the wet weights of rectus femoris muscles were assessed in this study, along with the protein levels of atrogin-1, p-PERK, Parkin and COXIV.Results: The wet weights of rectus femoris muscles, the protein levels of atrogin-1, p-PERK and Parkin increased after immobilization. It was also revealed that the protein levels of COXIV decreased after immobilization. Electrical stimulation was effective against muscle atrophy, the elevated expression of atrogin-1, p-PERK, Parkin, and the decreased expression of COXIV.Conclusions: Immobilization of unilateral lower limb could induce rectus femoris muscle atrophy, endoplasmic reticulum stress and Parkin mediated mitophagy. Endoplasmic reticulum stress-induced Parkin-dependent mitophagy may be one of the mechanisms by which electrical stimulation can play a significant role.

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Preventive effect and possible mechanisms of ultrashort wave diathermy on myogenic contracture in a rabbit model

Science Progress ◽

10.1177/00368504211054992 ◽

2021 ◽

Vol 104 (4) ◽

pp. 003685042110549

Author(s):

Qi-Yu Xu ◽

Quan-Bing Zhang ◽

Yun Zhou ◽

A-Ying Liu ◽

Feng Wang

Keyword(s):

Muscle Atrophy ◽

Myogenic Differentiation ◽

Rabbit Model ◽

Rectus Femoris ◽

Control Group ◽

Preventive Effect ◽

Cross Sectional ◽

Protein Levels ◽

Group I ◽

Ultrashort Wave

The purpose of this study was to determine the preventive effect of ultrashort wave diathermy on immobilization-induced myogenic contracture and to explore its underlying mechanisms. Forty-two rabbits were randomly assigned into control (Group C), immobilization (Group I, which was further divided into one week, Group I-1; two weeks, Group I-2; and four weeks, Group I-4, subgroups by the length of immobilization) and ultrashort wave prevention (Group U, which was further divided into one week, Group U-1; two weeks, Group U-2; and four weeks, Group U-4, by time of treatment) groups. Intervention effects were assessed by evaluating rectus femoris cross-sectional area (CSA), knee range of motion, and the protein levels for myogenic differentiation (MyoD) and muscle atrophy F-box (MAFbx-1) in the rectus femoris. Compared with those of Group C, in Groups I and U, total contracture, myogenic contracture, MyoD and MAFbx-1 levels were significantly elevated, and CSA was significantly smaller ( p < 0.05). Compared with those of Group I at each time point, MyoD levels were significantly elevated, MAFbx-1 levels were significantly lower, CSA was significantly larger, and myogenic contracture was significantly alleviated in Group U ( p < 0.05). In the early stages of contracture, ultrashort wave diathermy reduces muscle atrophy and delays the process of myogenic contracture during joint immobilization; the mechanism of this may be explained as increased expression of MyoD triggered by suppression of the MAFbx-1-mediated ubiquitin-proteasome pathway.

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Effect of Ultrashort Wave on Joint Dysfunction and Muscle Atrophy in a Rabbit Model of Extending Knee Joint Contracture: Enhanced Expression of MyoD

10.21203/rs.2.11412/v1 ◽

2019 ◽

Author(s):

Feng Wang ◽

Yun Zhou ◽

Quan Bing Zhang ◽

A Ying Liu ◽

Hua Zhang Zhong ◽

...

Keyword(s):

Knee Joint ◽

Muscle Atrophy ◽

Rabbit Model ◽

Rectus Femoris ◽

Joint Contracture ◽

Passive State ◽

Control Group ◽

Wave Treatment ◽

Protein Levels ◽

Ultrashort Wave

Abstract Background As a common clinical disease, the incidence of joint contracture which is characterized by the reduction of range of motion (ROM) in the active or passive state of the joint has increased in recent years. This study was to investigate the effects of ultrashort wave on joint dysfunction and muscle atrophy in a rabbit model of extending knee joint contracture and its mechanism. Methods 35 rabbits underwent unilateral immobilization of a knee joint at full extension to cause joint contracture, and 5 rabbits were used for the control group. After 8 weeks immobilization, 35 rabbits were randomly divided into the following seven groups: I-8, R-1, R-2, R-4, T-1, T-2, and T-4. In the Group R-1, R-2 and R-4, the rabbits were experienced one, two, and four weeks self-recovery. In the Group T-1, T-2, and T-4, the rabbits were experienced one, two, and four weeks ultrashort wave treatment. The effect of self-recovery and ultrashort wave treatment on joint dysfunction and muscle atrophy was assessed by measuring the degree of total and myogenic contracture, evaluating the cross-sectional area (CSA) of rectus femoris and assessing the protein levels for MyoD. Results A tendency toward reduced the degree of total and myogenic contracture was observed after self-recovery and ultrashort wave treatment. A tendency toward increased the CSA of rectus femoris and the protein levels for MyoD was observed after self-recovery and ultrashort wave treatment. The ultrashort wave treatment led a better efficacy than self-recovery against the total and the myogenic contracture, the CSA and the protein levels for MyoD of rectus femoris. Conclusions Ultrashort wave ameliorates joint dysfunction and muscle atrophy via upregulating the expression of MyoD protein in a rabbit model of extending knee joint contracture.

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MODY Signal Pathway in the Endoplasmic Reticulum Stress and the Role of Nkx6.1 in the Glucolipotoxicity of INS-1-3 Cells

Diabetes ◽

10.2337/db18-2110-p ◽

2018 ◽

Vol 67 (Supplement 1) ◽

pp. 2110-P

Author(s):

YANAN DONG ◽

YUKUN LI ◽

JIANZHONG XIAO

Keyword(s):

Endoplasmic Reticulum ◽

Endoplasmic Reticulum Stress ◽

Signal Pathway

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Molecular Targets of Manganese-Induced Neurotoxicity: A Five-Year Update

International Journal of Molecular Sciences ◽

10.3390/ijms22094646 ◽

2021 ◽

Vol 22 (9) ◽

pp. 4646

Author(s):

Alexey A. Tinkov ◽

Monica M. B. Paoliello ◽

Aksana N. Mazilina ◽

Anatoly V. Skalny ◽

Airton C. Martins ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Endoplasmic Reticulum Stress ◽

Mitochondrial Dysfunction ◽

Synaptic Dysfunction ◽

Future Research ◽

Protective Mechanism ◽

Autophagic Flux ◽

Future Research Directions ◽

The Impact

Understanding of the immediate mechanisms of Mn-induced neurotoxicity is rapidly evolving. We seek to provide a summary of recent findings in the field, with an emphasis to clarify existing gaps and future research directions. We provide, here, a brief review of pertinent discoveries related to Mn-induced neurotoxicity research from the last five years. Significant progress was achieved in understanding the role of Mn transporters, such as SLC39A14, SLC39A8, and SLC30A10, in the regulation of systemic and brain manganese handling. Genetic analysis identified multiple metabolic pathways that could be considered as Mn neurotoxicity targets, including oxidative stress, endoplasmic reticulum stress, apoptosis, neuroinflammation, cell signaling pathways, and interference with neurotransmitter metabolism, to name a few. Recent findings have also demonstrated the impact of Mn exposure on transcriptional regulation of these pathways. There is a significant role of autophagy as a protective mechanism against cytotoxic Mn neurotoxicity, yet also a role for Mn to induce autophagic flux itself and autophagic dysfunction under conditions of decreased Mn bioavailability. This ambivalent role may be at the crossroad of mitochondrial dysfunction, endoplasmic reticulum stress, and apoptosis. Yet very recent evidence suggests Mn can have toxic impacts below the no observed adverse effect of Mn-induced mitochondrial dysfunction. The impact of Mn exposure on supramolecular complexes SNARE and NLRP3 inflammasome greatly contributes to Mn-induced synaptic dysfunction and neuroinflammation, respectively. The aforementioned effects might be at least partially mediated by the impact of Mn on α-synuclein accumulation. In addition to Mn-induced synaptic dysfunction, impaired neurotransmission is shown to be mediated by the effects of Mn on neurotransmitter systems and their complex interplay. Although multiple novel mechanisms have been highlighted, additional studies are required to identify the critical targets of Mn-induced neurotoxicity.

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AMPA induced cognitive impairment in rats: Establishing the role of endoplasmic reticulum stress inhibitor, 4‐PBA

Journal of Neuroscience Research ◽

10.1002/jnr.24859 ◽

2021 ◽

Author(s):

Ankita Bhardwaj ◽

Rishi Bhardwaj ◽

Shweta Sharma ◽

Suresh Kumar Sharma ◽

Devinder Kumar Dhawan ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Cognitive Impairment ◽

Endoplasmic Reticulum Stress

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The Role of Endoplasmic Reticulum Stress and NLRP3 Inflammasomes in the Development of Atherosclerosis

Cytology and Genetics ◽

10.3103/s0095452721040113 ◽

2021 ◽

Vol 55 (4) ◽

pp. 331-339

Author(s):

V. V. Pushkarev ◽

L. K. Sokolova ◽

O. I. Kovzun ◽

V. M. Pushkarev ◽

M. D. Tronko

Keyword(s):

Endoplasmic Reticulum ◽

Endoplasmic Reticulum Stress ◽

Nlrp3 Inflammasomes

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Role of mTOR1 and mTOR2 complexes in MEG-01 cell physiology

Thrombosis and Haemostasis ◽

10.1160/th14-09-0727 ◽

2015 ◽

Vol 114 (11) ◽

pp. 969-981 ◽

Cited By ~ 4

Author(s):

Esther López ◽

Alejandro Berna-Erro ◽

Javier J. López ◽

María P. Granados ◽

Nuria Bermejo ◽

...

Keyword(s):

Cell Proliferation ◽

Endoplasmic Reticulum ◽

Endoplasmic Reticulum Stress ◽

Mammalian Target Of Rapamycin ◽

Target Of Rapamycin ◽

Cell Physiology ◽

Cell Stimulation ◽

Intracellular Location ◽

Macromolecular Complexes

SummaryThe function of the mammalian target of rapamycin (mTOR) is upregulated in response to cell stimulation with growing and differentiating factors. Active mTOR controls cell proliferation, differentiation and death. Since mTOR associates with different proteins to form two functional macromolecular complexes, we aimed to investigate the role of the mTORI and mTOR2 complexes in MEG-01 cell physiology in response to thrombopoietin (TPO). By using mTOR antagonists and overexpressing FKBP38, we have explored the role of both mTOR complexes in proliferation, apoptosis, maturation-like mechanisms, endoplasmic reticulum-stress and the intracellular location of both active mTOR complexes during MEG-01 cell stimulation with TPO. The results demonstrate that mTOR1 and mTOR2 complexes play different roles in the physiology of MEG-01 cells and in the maturation-like mechanisms; hence, these findings might help to understand the mechanism underlying generation of platelets.

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