<scp>NF</scp>‐<scp>KB</scp> activity functions in primary pericytes in a cell‐ and non‐cell‐autonomous manner to affect myotube formation

Hyldahl, Robert D.; Schwartz, Lawrence M.; Clarkson, Priscilla M.

doi:10.1002/mus.23640

Cited by 12 publications

(8 citation statements)

References 44 publications

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“…Additionally, we recently demonstrated that cells within the vascular region of the ECM (pericytes) activate the transcription factor NF‐kB in response to eccentric exercise . Follow‐up analyses of this result indicated that pericyte‐derived NF‐kB activity may function to promote satellite cell proliferation . Thus, it is becoming apparent that interactions between myofibers and multiple ECM compartments play a fundamental role in the molecular response to eccentric stress.…”

Section: Do Eccentric Contractions Cause Damage In Healthy Muscle?mentioning

confidence: 99%

Lengthening our perspective: Morphological, cellular, and molecular responses to eccentric exercise

2013

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The response of skeletal muscle to unaccustomed eccentric exercise has been studied widely, yet it is incompletely understood. This review is intended to provide an up-to-date overview of our understanding of how skeletal muscle responds to eccentric actions, with particular emphasis on the underlying molecular and cellular mechanisms of damage and recovery. This review begins by addressing the question of whether eccentric actions result in physical damage to muscle fibers and/or connective tissue. We next review the symptomatic manifestations of eccentric exercise (i.e., indirect damage markers, such as delayed onset muscle soreness), with emphasis on their relatively poorly understood molecular underpinnings. We then highlight factors that potentially modify the muscle damage response following eccentric exercise. Finally, we explore the utility of using eccentric training to improve muscle function in populations of healthy and aging individuals, as well as those living with neuromuscular disorders.

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Section: Do Eccentric Contractions Cause Damage In Healthy Muscle?mentioning

confidence: 99%

Lengthening our perspective: Morphological, cellular, and molecular responses to eccentric exercise

2013

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“…For example, intramuscular mechanical pressure during EIMD is transferred through the extracellular matrix inducing an early release of growth factors from fibroblasts that result in the activation of adjacent satellite cell populations via selective intracellular signaling pathways which may promote muscle healing 51,52. Vascular cells such as pericytes are also involved in EIMD by activating nuclear factor-kappa B (NF-κB) signaling which is implicated in immune cell mobilization and satellite cell proliferation 7,53,54. However, it must be mentioned that NF-κB pathway mediates the upregulation of the activity of the ubiquitin–proteosome system (UPS) by proinflammatory cytokines (i.e., tumor necrosis factor-alpha [TNF-α] and interleukin-6 [IL-6]) thereby contributing to protein degradation of skeletal muscle proteins and overall EIMD 55.…”

Section: Mechanisms and Consequencesmentioning

confidence: 99%

Insights into the molecular etiology of exercise-induced inflammation: opportunities for optimizing performance

Fatouros

Jamurtas

2016

JIR

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The study of exercise-induced muscle damage (EIMD) is of paramount importance not only because it affects athletic performance but also because it is an excellent model to study the mechanisms governing muscle cachexia under various clinical conditions. Although, a large number of studies have investigated EIMD and its associated inflammatory response, several aspects of skeletal muscles responses remain unclear. In the first section of this article, the mechanisms of EIMD are reviewed in an attempt to follow the events that result in functional and structural alterations of skeletal muscle. In the second section, the inflammatory response associated with EIMD is presented with emphasis in leukocyte accumulation through mechanisms that are largely coordinated by pro- and anti-inflammatory cytokines released either by injured muscle itself or other cells. The practical applications of EIMD and the subsequent inflammatory response are discussed with respect to athletic performance. Specifically, the mechanisms leading to performance deterioration and development of muscle soreness are discussed. Emphasis is given to the factors affecting individual responses to EIMD and the resulting interindividual variability to this phenomenon.

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“…Nuclear factor-κB (NF-κB) is a nuclear transcription factor that regulates the expression of a large number of genes associated with inflammation [1,2], tissue damage and repair [3,4], cell differentiation [5,6], apoptosis [7,8] and tumor growth [9,10]. NF-κB is composed of five distinct but structurally related subunits: RelA, RelB, c-Rel, p50 and p52, and these five mature proteins can form various homodimeric and heterodimeric combinations [11,12].…”

Section: Introductionmentioning

confidence: 99%

NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells

Zhang

et al. 2014

J Transl Med

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BackgroundNuclear factor-κB (NF-κB) induces a variety of biological processes through transcriptional gene control whose products are components in various signaling pathways. MicroRNAs are a small endogenous non-coding RNAs that regulate gene expression and are involved in tumorigenesis. Using human cervical cancer cell lines, this study aimed to investigate whether NF-κB could regulate miR-130a expression and the functions and targets of miR-130a.MethodsWe used the HeLa and C33A cervical cancer cell lines that were transfected with NF-κB or miR-130a overexpression plasmids to evaluate their effects on cell growth. We utilized bioinformatics, a fluorescent reporter assay, qRT-PCR and Western blotting to identify downstream target genes.ResultsIn HeLa and C33A cells, NF-κB and miR-130a overexpression promoted cell growth, but genetic knockdowns suppressed growth. TNF-α was identified as a target of miR-130a by binding in a 3’-untranslated region (3’UTR) EGFP reporter assay and by Western blot analysis. Furthermore, low TNF-α concentrations stimulated NF-κB activity and then induced miR-130a expression, and TNF-α overexpression rescued the effects of miR-130a on cervical cancer cells.ConclusionsOur findings indicate that TNF-α can activate NF-κB activity, which can reduce miR-130a expression, and that miR-130a targets and downregulates TNF-α expression. Hence, we shed light on the negative feedback regulation of NF-κB/miR-130a/TNF-α/NF-κB in cervical cancer and may provide insight into the carcinogenesis of cervical cancer.

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NF‐KB activity functions in primary pericytes in a cell‐ and non‐cell‐autonomous manner to affect myotube formation

Abstract: NF-kB activity acts cell-autonomously to inhibit HPP myogenic differentiation and non-cell-autonomously to promote MPC proliferation and suppress MPC differentiation in vitro.

Cited by 12 publications

References 44 publications

Lengthening our perspective: Morphological, cellular, and molecular responses to eccentric exercise

Lengthening our perspective: Morphological, cellular, and molecular responses to eccentric exercise

Insights into the molecular etiology of exercise-induced inflammation: opportunities for optimizing performance

NF-κB-modulated miR-130a targets TNF-α in cervical cancer cells

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