The antioxidant requirement for plasma membrane repair in skeletal muscle

Labazi, M.; McNeil, Anna K.; Kurtz, Timothy; Lee, Taylor C.; Pegg, Ronald B.; Angeli, José Pedro Friedmann; Conrad, Marcus; McNeil, Paul L.

doi:10.1016/j.freeradbiomed.2015.03.016

Cited by 36 publications

(52 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This process requires GSH that gives an electron, leading to the formation of oxidized GSH. Vitamin E is required for skeletal muscle plasma membrane repair (141,176). However, the underlying cellular and molecular mechanisms of this phenomenon remain to be determined (166).…”

Section: B Exogenousmentioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

152

120

View full text Add to dashboard Cite

Skeletal muscle shows high plasticity in response to external demand. Moreover, adult skeletal muscle is capable of complete regeneration after injury, due to the properties of muscle stem cells (MuSCs), the satellite cells, which follow a tightly regulated myogenic program to generate both new myofibers and new MuSCs for further needs. Although reactive oxygen species (ROS) and reactive nitrogen species (RNS) have long been associated with skeletal muscle physiology, their implication in the cell and molecular processes at work during muscle regeneration is more recent. This review focuses on redox regulation during skeletal muscle regeneration. An overview of the basics of ROS/RNS and antioxidant chemistry and biology occurring in skeletal muscle is first provided. Then, the comprehensive knowledge on redox regulation of MuSCs and their surrounding cell partners (macrophages, endothelial cells) during skeletal muscle regeneration is presented in normal muscle and in specific physiological (exercise-induced muscle damage, aging) and pathological (muscular dystrophies) contexts. Recent advances in the comprehension of these processes has led to the development of therapeutic assays using antioxidant supplementation, which result in inconsistent efficiency, underlying the need for new tools that are aimed at precisely deciphering and targeting ROS networks. This review should provide an overall insight of the redox regulation of skeletal muscle regeneration while highlighting the limits of the use of nonspecific antioxidants to improve muscle function. Antioxid. Redox Signal. 27, 276-310.

show abstract

Section: B Exogenousmentioning

confidence: 99%

Redox Control of Skeletal Muscle Regeneration

Moal

Pialoux

Juban

et al. 2017

Antioxidants & Redox Signaling

152

120

View full text Add to dashboard Cite

show abstract

“…In many cell types, such as myocytes, physiological mechanical loading (e.g., treadmill exercise for the musculoskeletal system) creates tears in the cell membrane called plasma membrane disruptions (PMD) . These survivable, nanometer‐ to micron‐sized tears promote molecular flux across the cell membrane, allowing Ca 2+ entry and release of growth factors like FGFs .…”

mentioning

confidence: 99%

Mechanical loading disrupts osteocyte plasma membranes which initiates mechanosensation events in bone

Sellman

Bahraini

et al. 2017

Journal Orthopaedic Research

Self Cite

View full text Add to dashboard Cite

Osteocytes sense loading in bone, but their mechanosensation mechanisms remain poorly understood. Plasma membrane disruptions (PMD) develop with loading under physiological conditions in many cell types (e.g., myocytes, endothelial cells). These PMD foster molecular flux across cell membranes that promotes tissue adaptation, but this mechanosensation mechanism had not been explored in osteocytes. Our goal was to investigate whether PMD occur and initiate consequent mechanotransduction in osteocytes during physiological loading. We found that osteocytes experience PMD during in vitro (fluid flow) and in vivo (treadmill exercise) mechanical loading, in proportion to the level of stress experienced. In fluid flow studies, osteocyte PMD preferentially formed with rapid as compared to gradual application of loading. In treadmill studies, osteocyte PMD increased with loading in weight bearing locations (tibia), but this trend was not seen in non-weight bearing locations (skull). PMD initiated osteocyte mechanotransduction including calcium signaling and expression of c-fos, and repair rates of these PMD could be enhanced or inhibited pharmacologically to alter downstream mechanotransduction and osteocyte survival. PMD may represent a novel mechanosensation pathway in bone and a target for modifying skeletal adaptation signaling in osteocytes. © 2017 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:653-662, 2018.

show abstract

“…Therefore, the location of ROS production after plasma membrane injury as well as the extent to which it is produced can have seemingly contradictory effects on the ability of cells to repair membrane damage. Of interest in this regard is the observation that plasma membrane-directed glutathione peroxidase 4 (Gpx4) aids in repair, suggesting that plasma membrane lipid peroxidation inhibits repair [120]. This observation is supported by the ability of vitamin E, a membrane localized antioxidant, to improve plasma membrane repair, while the cytosolic antioxidant N-acetyl cysteine (NAC) does not affect repair [112].…”

Section: Signals and Effectors Of Plasma Membrane Repairmentioning

confidence: 99%

“…This potentially ties ROS signaling back into calcium-dependent repair signaling. Other studies investigating more general, globally acting antioxidants, such as DTT and melatonin, conclude they are detrimental to repair [109,110,120]. Thus, involvement of lipid oxidation in membrane repair does not appear to be straightforward.…”

Section: Signals and Effectors Of Plasma Membrane Repairmentioning

confidence: 99%

Cellular mechanisms and signals that coordinate plasma membrane repair

Horn

Jaiswal

2018

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Plasma membrane forms the barrier between the cytoplasm and the environment. Cells constantly and selectively transport molecules across their plasma membrane without disrupting it. Any disruption in the plasma membrane compromises its selective permeability and is lethal, if not rapidly repaired. There is a growing understanding of the organelles, proteins, lipids, and small molecules that help cells signal and efficiently coordinate plasma membrane repair. This review aims to summarize how these subcellular responses are coordinated and how cellular signals generated due to plasma membrane injury interact with each other to spatially and temporally coordinate repair. With the involvement of calcium and redox signaling in single cell and tissue repair, we will discuss how these and other related signals extend from single cell repair to tissue level repair. These signals link repair processes that are activated immediately after plasma membrane injury with longer term processes regulating repair and regeneration of the damaged tissue. We propose that investigating cell and tissue repair as part of a continuum of wound repair mechanisms would be of value in treating degenerative diseases.

show abstract

The antioxidant requirement for plasma membrane repair in skeletal muscle

Cited by 36 publications

References 53 publications

Redox Control of Skeletal Muscle Regeneration

Redox Control of Skeletal Muscle Regeneration

Mechanical loading disrupts osteocyte plasma membranes which initiates mechanosensation events in bone

Cellular mechanisms and signals that coordinate plasma membrane repair

Contact Info

Product

Resources

About