Whole-body-vibration training positively affects muscle transcriptome in tumour bearing cachectic mice
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PROVIDER: PRJNA501868 | ENA |
REPOSITORIES: ENA
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Project description:Background The prevailing view is that a combination of nutritional, pharmacological and exercise therapy is most optimal to reduce the development and progression of cancer cachexia. However, in many cancer patients, physical activity is hampered by frailty and fatigue. The present study aimed to investigate whole-body vibration training (WBV) as potential alternative to attenuate loss of weight, muscle mass and function in tumour bearing mice. Methods Twenty-four male CD2F1-mice (21.5±0.2g) were stratified into four groups (control=[C], control+WBV=[C+V], tumour-bearing=[T] and tumour-bearing+WBV=[T+V]), and injected (day 1) with C26 cells or vehicle. From day 1, whole-body-vibration (WBV groups) was performed for 19 days (15min, 45Hz, 1.0g acceleration). General outcome measures included body mass and composition, and daily activity. In addition, blood analysis and assessments of muscle histology and function and whole genome gene expression in m. soleus (SOL) and m. extensor digitorum longus (EDL) were performed. Two-way ANOVA with factors tumour, training and interaction was used for statistical analysis. Results Body weight, lean and fat mass and EDL mass were all lower in tumour bearing mice compared to controls. No effects of vibration training were found on systemic cachexia related outcomes. However, WBV increased EDL mass in the control treatment,. SOL mass did not differ, whereas SOL function was affected by both tumour and WBV. Interestingly, WBV reduced the tumour-related effects on muscle gene expression in EDL, SOL and heart. Conclusions These data suggest that WBV had only minor effects on cachexia related outcomes in the present experimental set-up, while muscle transcriptome was positively affected. This merits follow-up studies applying for example longer treatment periods or incorporating WBV in a multiple-target intervention.
2020-11-01 | GSE121972 | GEO
Project description:To investigate which factors might be driving the cachectic muscle wasting observed in our larval models bearing RasV12, scrib1 tumors, we performed RNA sequencing (RNAseq) on the cuticles of wild type and RasV12, scrib1 tumour-bearing larvae. Pathway and gene ontology analysis revealed significant deregulation of stress and starvation response genes, metabolic genes, and inflammation and immune regulatory genes within cachectic muscle of tumour bearing larvae.
2021-06-17 | GSE178332 | GEO
Project description:We found out that bile acid pathways were deeply altered in cachectic mice bearing ectopic tumor, leading to an increase in portal and liver conjugated bile acid levels. Counteracting this increased level in conjugated bile acids using cholestyramine, a bile acid sequestrant, reduced hepatic inflammation in cachectic mice with no impact on steatosis and minor effects on thermogenesis. Hepatic whole transcriptome analysis identified 16 pathways altered in cachectic mice which were counteracted by cholestyramine, pointing out the large contribution of bile acids to hepatic disturbances occurring in cancer cachexia.
2021-02-24 | GSE154219 | GEO
Project description:RNA sequencing analysis of muscles comparing normal muscles with cachectic muscles isolated from mice bearing distant metastasis from C26m2 and 4T1 murine colon and breast cancer cell lines, collected at the onset of weight loss five weeks after tumor cell injection in these mice.
2018-07-01 | GSE112204 | GEO
Project description:Background: Anorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation. Methods: Two tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips). Results: In both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion. Conclusions: Altered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.
2014-10-31 | GSE57189 | GEO
Project description:Background: Anorexia is a common symptom among cancer patients and contributes to malnutrition and strongly impinges on quality of life. Cancer-induced anorexia is thought to be caused by an inability of food intake-regulating systems in the hypothalamus to respond adequately to negative energy balance during tumour growth. Here, we show that this impaired response of food-intake control is likely to be mediated by altered serotonin signalling and by failure in post-transcriptional neuropeptide Y (NPY) regulation. Methods: Two tumour cachectic mouse models with different food intake behaviours were used: a C26-colon adenocarcinoma model with increased food intake and a Lewis lung carcinoma model with decreased food intake. This contrast in food intake behaviour between tumour-bearing (TB) mice in response to growth of the two different tumours was used to distinguish between processes involved in cachexia and mechanisms that might be important in food intake regulation. The hypothalamus was used for transcriptomics (affymetrix chips). Results: In both models, hypothalamic expression of orexigenic NPY was significantly higher compared with controls, suggesting that this change does not directly reflect food intake status but might be linked to negative energy balance in cachexia. Expression of genes involved in serotonin signalling showed to be different between C26-TB mice and Lewis lung carcinoma-TB mice and was inversely associated with food intake. In vitro, using hypothalamic cell lines, serotonin repressed neuronal hypothalamic NPY secretion while not affecting messenger NPY expression, suggesting that serotonin signalling can interfere with NPY synthesis, transport, or secretion. Conclusions: Altered serotonin signalling is associated with changes in food intake behaviour in cachectic TB mice. Serotonins' inhibitory effect on food intake under cancer cachectic conditions is probably via affecting the NPY system. Therefore, serotonin regulation might be a therapeutic target to prevent the development of cancer-induced eating disorders.
2014-10-31 | GSE57188 | GEO
Project description:A regular physical training is known to contribute to preserve muscle mass and strength, maintaining structure and function of neural and vascular compartments and preventing muscle insulin resistance and inflammation. However, physical activity is progressively reduced during aging causing mobility limitations and poor quality of life. Although physical exercise for rehabilitation purposes (e.g., after fractures or cardiovascular events) or simply aiming to counteract the development of sarcopenia is frequently advised by physicians, nevertheless few data are available on the targets and the global effects on the muscle organ of adapted exercise especially if started at old age. To contribute answering this question for medical translational purposes, the proteomic profile of the gastrocnemius muscle was analyzed in 24-month-old mice undergoing adapted physical training on a treadmill for 12 weeks or kept under a sedentary lifestyle condition. Proteomic data were implemented by morphological and morphometrical ultrastructural evaluations. Data demonstrate that muscles can respond to adapted physical training started at old age, positively modulating their morphology and the proteomic profile fostering protective and saving mechanisms either involving muscle cell components and pathways (i.e., mitochondrial processes, translation pathways and protein refolding, contractile apparatus) as well as the extracellular compartment. Therefore, this study provides important insights on the targets of adapted physical training, which can be regarded as suitable benchmarks for future in vivo studies further exploring the effects of this type of physical activity by functional/metabolic approaches.
2023-11-06 | PXD045483 | Pride
Project description:Targeted exercise combined with nutritional and pharmacological strategies is commonly considered to be the most optimal strategy to reduce the development and progression of cachexia. For COPD patients, this multi-targeted treatment has shown beneficial effects. However, in many, physical activity is seriously hampered by frailty and fatigue. In the present study, effects of whole-body-vibration-training (WBV) were investigated, as potential alternative to active exercise, on body mass, muscle mass and function in tumour bearing mice. Twenty-four male CD2F1-mice (6–8 weeks, 21.5 ± 0.2 g) were stratified into four groups: control, control + WBV, C26 tumour-bearing, and C26 tumour-bearing + WBV. From day 1, whole-body-vibration was daily performed for 19 days (15 min, 45 Hz, 1.0 g acceleration). General outcome measures included body mass and composition, daily activity, blood analysis, assessments of muscle histology, function, and whole genome gene expression in m. soleus (SOL), m. extensor digitorum longus (EDL), and heart. Body mass, lean and fat mass and EDL mass were all lower in tumour bearing mice compared to controls. Except from improved contractility in SOL, no effects of vibration training were found on cachexia related general outcomes in control or tumour groups, as PCA analysis did not result in a distinction between corresponding groups. However, analysis of transcriptome data clearly revealed a distinction between tumour and trained tumour groups. WBV reduced the tumour-related effects on muscle gene expression in EDL, SOL and heart. Gene Set Enrichment Analysis showed that these effects were associated with attenuation of the upregulation of the proteasome pathway in SOL. These data suggest that WBV had minor effects on cachexia related general outcomes in the present experimental set-up, while muscle transcriptome showed changes associated with positive effects. This calls for follow-up studies applying longer treatment periods of WBV as component of a multiple-target intervention.
| S-EPMC8566567 | biostudies-literature
Project description:Brain expression profiling of bees perfroming consistently vibration signal (modulatory signal that stimulates the performance of several different activities in the hive).
2009-07-01 | E-TABM-608 | biostudies-arrayexpress
Project description:Cancer mediated activation of the ActRIIB-ALK4/5 heterodimer by myostatin is strongly associated with muscle wasting. Progressive skeletal muscle wasting, with or without loss of adipose tissue, is observed in up to 50 per cent of all cancer patients. This multifactorial syndrome is known as cachexia, and cannot be fully reversed by conventional nutritional support. Cachexia leads to progressive functional impairment. We investigated in vitro and in vivo the efficacy of ALK4/5 receptor blockers like SB431542 in preventing muscle wasting and in this context determined muscle-related miRNA expression profiles in non-tumor bearing control mice, in SB431542 treated C26 tumor-bearing mice and in cachectic C26 tumor-bearing mice.
2018-09-28 | GSE120593 | GEO