MicroRNA expression and protein acetylation pattern in respiratory and limb muscles of Parp-1−/− and Parp-2−/− mice with lung cancer cachexia

Chacon-Cabrera, Alba; Fermoselle, Clara; Salmela, Ida; Yélamos, José; Barreiro, Esther

doi:10.1016/j.bbagen.2015.09.020

Cited by 46 publications

(133 citation statements)

References 60 publications

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“…MyHC-I and MyHC-II isoforms were identified using anti-MyHC-I (clone MHC, Biogenesis Inc., Poole, England, UK) and anti-MyHC-II antibodies (clone MY-32, Sigma, Saint Louis, MO), respectively, according to previously published methodologies [4, 6–8, 18]. …”

Section: Methodsmentioning

confidence: 99%

“…The area fraction of normal and abnormal muscle was evaluated on 3 μm paraffin-embedded sections of the diaphragm and gastrocnemius muscles in all groups of mice following previously published methodologies [4, 6–8, 16]. …”

Section: Methodsmentioning

confidence: 99%

“…In muscle paraffin-embedded sections, apoptotic nuclei were identified using the TUNEL assay (In Situ Cell Death Detection Kit, POD, Roche Applied Science, Mannheim, Germany) in both diaphragm and gastrocnemius muscle specimens from all study groups following the manufacturer’s instructions and previous studies [6–8, 44]. In each muscle preparation, altered fibers were expressed as the ratio of total TUNEL positively-stained nuclei to the total number of counted nuclei, as also previously described [6–8, 44].…”

Section: Methodsmentioning

confidence: 99%

“…In each muscle preparation, altered fibers were expressed as the ratio of total TUNEL positively-stained nuclei to the total number of counted nuclei, as also previously described [6–8, 44]. A minimum amount of 300 nuclei were counted in each muscle preparation.…”

Section: Methodsmentioning

confidence: 99%

“…Importantly, the experimental models of cachexia in which the underlying biological mechanisms have been identified so far were mostly characterized by a subacute exposure of the animals to a large burden of different cancer cell types that led to a rapid muscle mass loss with implications in total body weight [7, 8, 14, 42]. Whether similar features in skeletal muscles are to be expected in a chronic model of lung carcinogenesis, which may mimic more closely the human disease, remains to be answered.…”

Section: Introductionmentioning

confidence: 99%

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Phenotypic and metabolic features of mouse diaphragm and gastrocnemius muscles in chronic lung carcinogenesis: influence of underlying emphysema

et al. 2016

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BackgroundMuscle wasting negatively impacts the progress of chronic diseases such as lung cancer (LC) and emphysema, which are in turn interrelated.ObjectivesWe hypothesized that muscle atrophy and body weight loss may develop in an experimental mouse model of lung carcinogenesis, that the profile of alterations in muscle fiber phenotype (fiber type composition and morphometry, muscle structural alterations, and nuclear apoptosis), and in muscle metabolism are similar in both respiratory and limb muscles of the tumor-bearing mice, and that the presence of underlying emphysema may influence those events.MethodsDiaphragm and gastrocnemius muscles of mice with urethane-induced lung cancer (LC-U) with and without elastase-induced emphysema (E–U) and non-exposed controls (N = 8/group) were studied: fiber type composition, morphometry, muscle abnormalities, apoptotic nuclei (immunohistochemistry), and proteolytic and autophagy markers (immunoblotting) at 20- and 35-week exposure times. In the latter cohort, structural contractile proteins, creatine kinase (CK), peroxisome proliferator-activated receptor (PPAR) expression, oxidative stress, and inflammation were also measured. Body and muscle weights were quantified (baseline, during follow-up, and sacrifice).ResultsCompared to controls, in U and E–U mice, whole body, diaphragm and gastrocnemius weights were reduced. Additionally, both in diaphragm and gastrocnemius, muscle fiber cross-sectional areas were smaller, structural abnormalities, autophagy and apoptotic nuclei were increased, while levels of actin, myosin, CK, PPARs, and antioxidants were decreased, and muscle proteolytic markers did not vary among groups.ConclusionsIn this model of lung carcinogenesis with and without emphysema, reduced body weight gain and muscle atrophy were observed in respiratory and limb muscles of mice after 20- and 35-week exposure times most likely through increased nuclear apoptosis and autophagy. Underlying emphysema induced a larger reduction in the size of slow- and fast-twitch fibers in the diaphragm of U and E–U mice probably as a result of the greater inspiratory burden imposed onto this muscle.Electronic supplementary materialThe online version of this article (doi:10.1186/s12967-016-1003-9) contains supplementary material, which is available to authorized users.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Phenotypic and metabolic features of mouse diaphragm and gastrocnemius muscles in chronic lung carcinogenesis: influence of underlying emphysema

et al. 2016

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Inflammatory Events and Oxidant Production in the Diaphragm, Gastrocnemius, and Blood of Rats Exposed to Chronic Intermittent Hypoxia: Therapeutic Strategies

Domínguez-Álvarez

Gea

Barreiro

2016

Journal Cellular Physiology

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We hypothesized that inflammatory events and reactive oxygen species (ROS) production may be differentially expressed in respiratory and limb muscles, and blood of a chronic intermittent hypoxia (CIH) experimental model and that antioxidants and TNF-alpha blockade may influence those events. In blood, diaphragm, and gastrocnemius of rats non-invasively exposed to CIH (10% hypoxia, 2 h/day, 14 consecutive days) with/without concomitant treatment with either anti-TNF-alpha antibody (infliximab) or N-acetyl cysteine (NAC), inflammatory cytokines, superoxide anion production, muscle structural abnormalities, and fiber-type composition were assessed. Compared to non-exposed controls, in CIH-exposed rats, body weight gain was reduced, TNF-alpha, IL-1beta, IL-6, and interferon-gamma levels were increased in diaphragm, TNF-alpha, and IL-1 beta plasma levels were greater, systemic and muscle superoxide anion production was higher, diaphragm and gastrocnemius inflammatory cells and internal nuclei were higher, and muscle fiber-type and morphometry remained unmodified. CIH rats treated with infliximab further increased TNF-alpha, IL-1beta, IL-6, and interferon-gamma diaphragm levels, whereas NAC induced a reduction only in TNF-alpha and IL-1beta levels in diaphragm and plasma. Infliximab and NAC elicited a significant decline in superoxide anion production in diaphragm, gastrocnemius, and plasma, while inducing a further increase in inflammatory cells and internal nuclei in both muscles. Proinflammatory cytokines are differentially expressed in respiratory and limb muscles and plasma of CIH-exposed rats, while superoxide anion production increased in both muscle types and blood. Infliximab and NAC exerted different effects. These findings may help understand the biology underlying CIH in skeletal muscles and blood of patients with chronic respiratory diseases. J. Cell. Physiol. 232: 1165-1175, 2017. © 2016 Wiley Periodicals, Inc.

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Short‐ and Long‐Term Hindlimb Immobilization and Reloading: Profile of Epigenetic Events in Gastrocnemius

Chacon-Cabrera

Gea

Barreiro

2016

Journal Cellular Physiology

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Skeletal muscle dysfunction and atrophy are characteristic features accompanying chronic conditions. Epigenetic events regulate muscle mass and function maintenance. We hypothesized that the pattern of epigenetic events (muscle-enriched microRNAs and histone acetylation) and acetylation of transcription factors known to signal muscle wasting may differ between early- and late-time points in skeletal muscles of mice exposed to hindlimb immobilization (I) and recovery following I. Body and muscle weights, grip strength, muscle-enriched microRNAs, histone deacetylases (HDACs), acetylation of proteins, histones, and transcription factors (TF), myogenic TF factors, and muscle phenotype were assessed in gastrocnemius of mice exposed to periods (1, 2, 3, 7, 15, and 30 days, I groups) of hindlimb immobilization, and in those exposed to reloading for different periods of time (1, 3, 7, 15, and 30 days, R groups) following 7-day immobilization. Compared to non-immobilized controls, muscle weight, limb strength, microRNAs, especially miR-486, SIRT1 levels, and slow- and fast-twitch cross-sectional areas were decreased in mice of I groups, whereas Pax7 and acetylated FoxO1 and FoxO3 levels were increased. Muscle reloading following splint removal improved muscle mass loss, strength, and fiber atrophy, by increasing microRNAs, particularly miR-486, and SIRT1 content, while decreasing acetylated FoxO1 and FoxO3 levels. In this mouse model of disuse muscle atrophy, muscle-enriched microRNAs, especially miR-486, through Pax7 regulation delayed muscle cell differentiation following unloading of gastrocnemius muscle. Acetylation of FoxO1 and 3 seemed to drive muscle mass loss and atrophy, while deacetylation of these factors through SIRT1 would enable the muscle fibers to regenerate. J. Cell. Physiol. 232: 1415-1427, 2017. © 2016 Wiley Periodicals, Inc.

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MicroRNA expression and protein acetylation pattern in respiratory and limb muscles of Parp-1−/− and Parp-2−/− mice with lung cancer cachexia

Cited by 46 publications

References 60 publications

Phenotypic and metabolic features of mouse diaphragm and gastrocnemius muscles in chronic lung carcinogenesis: influence of underlying emphysema

Phenotypic and metabolic features of mouse diaphragm and gastrocnemius muscles in chronic lung carcinogenesis: influence of underlying emphysema

Inflammatory Events and Oxidant Production in the Diaphragm, Gastrocnemius, and Blood of Rats Exposed to Chronic Intermittent Hypoxia: Therapeutic Strategies

Short‐ and Long‐Term Hindlimb Immobilization and Reloading: Profile of Epigenetic Events in Gastrocnemius

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