0000000000361819

AUTHOR

Mathias Mericskay

showing 3 related works from this author

0393: Impact of miR-378* and its target desmin intermediate filament on mitochondria distribution in cardiomyocytes

2014

Background MiR-378 and miR-378* microRNAs are derived from an intron of the PGC-1β gene, a regulator of mitochondrial biogenesis. Their expression is either repressed or increased during heart failure depending on the model. Through proteomics approaches, we previously identified new targets of these miRs in H9c2 fetal cardiomyoblasts, among which lactate dehydrogenase for miR-378 and key cytoskeletal proteins for miR-378*. Aims To better assess its role in energy metabolism and differentiation; we overexpressed miR-378 and miR-378* in primary neonate rat cardiomyocytes (NRC) that are more differentiated and less proliferative than H9c2 cardiomyoblasts. Results We identified desmin as a new…

business.industryCellMitochondrionBioinformaticsProteomicsCell biologymedicine.anatomical_structureMitochondrial biogenesismicroRNAMedicineDesminCardiology and Cardiovascular MedicinebusinessCytoskeletonIntermediate filamentArchives of Cardiovascular Diseases Supplements
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Aged Nicotinamide Riboside Kinase 2 Deficient Mice Present an Altered Response to Endurance Exercise Training

2018

Background: Skeletal muscle aging is marked by the development of a sarcopenic phenotype, a global decline of muscle energetic capacities, and an intolerance to exercise. Among the metabolic disorders involved in this syndrome, NAD metabolism was shown to be altered in skeletalmuscle, with an important role for the NAMPT enzyme recycling the nicotinamide precursor. An alternative pathway for NAD biosynthesis has been described for the nicotinamide riboside vitamin B3 precursor used by the NMRK kinases, including the striated muscle-specific NMRK2.Aim: With this study, our goal is to explore the ability of 16-month-old Nmrk2−/− mice to perform endurance exercise and study the consequences on…

exerciselcsh:QP1-981agingheartskeletal muscleNADNMRK2lcsh:PhysiologyFrontiers in Physiology
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Aerobic Exercise and Pharmacological Treatments Counteract Cachexia by Modulating Autophagy in Colon Cancer

2016

Recent studies have correlated physical activity with a better prognosis in cachectic patients, although the underlying mechanisms are not yet understood. In order to identify the pathways involved in the physical activity-mediated rescue of skeletal muscle mass and function, we investigated the effects of voluntary exercise on cachexia in colon carcinoma (C26)-bearing mice. Voluntary exercise prevented loss of muscle mass and function, ultimately increasing survival of C26-bearing mice. We found that the autophagic flux is overloaded in skeletal muscle of both colon carcinoma murine models and patients, but not in running C26-bearing mice, thus suggesting that exercise may release the auto…

0301 basic medicineCachexiaColorectal cancerMuscle Fibers SkeletalMicevoluntary physical activityChloroquineMice Inbred BALB CMultidisciplinaryMuscle WeaknessMyogenesis3. Good healthmedicine.anatomical_structureColonic NeoplasmsFemalecancer cachexiamedicine.drugmedicine.medical_specialty[SDV.CAN]Life Sciences [q-bio]/Cancerautophagic fluxBiologyArticleCachexia03 medical and health sciencesAtrophyInternal medicineCell Line TumorPhysical Conditioning AnimalmedicineAutophagyAerobic exerciseAnimalsHumansMuscle SkeletalSirolimusrapamycinAutophagyAutophagosomesSkeletal musclemuscle wasting[SDV.MHEP.HEG]Life Sciences [q-bio]/Human health and pathology/Hépatology and GastroenterologyRibonucleotidesmedicine.diseaseAminoimidazole CarboxamideSurvival Analysisexercise mimetics030104 developmental biologyEndocrinology5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR)LysosomesNeoplasm Transplantationmuscle wasting; cancer cachexia; voluntary physical activity; exercise mimetics; 5-amino-1-beta-D-ribofuranosyl-imidazole-4-carboxamide (AICAR); rapamycin; autophagic flux
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