Metabolomics Workbench ST000671 - GNPS - LCR/HCR rat mitochondrial study
Ontology highlight
ABSTRACT:
INSTRUMENT(S): QTOF - NEGATIVE, QTOF - POSITIVE
ORGANISM(S): Rattus Norvegicus
SUBMITTER: 
Maureen Kachman
PROVIDER: MSV000082712 | GNPS | Thu Aug 02 17:16:00 BST 2018
REPOSITORIES: GNPS
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Project description:LCR and HCR rats (from Nathan Qi's 2010 study) were dissected at rest or following 10 minutes of exercise. Mitochondria were isolated from frozen gastrocnemius skeletal muscle. Samples consist of these isolated mitochondria suspended in 50 uL of mitochondrial isolation buffer (IBM containing sucrose, salts, etc; see Katie Overmyer's notebook E, p~23).
2017-06-05 | ST000671 | MetabolomicsWorkbench
Project description:We performed transcutaneous electrode stimulation to the tibialis anterior (TA) muscle of rats to mimic resistance exercise and mass spectrometer to measure the changes in protein expression following exercise. Wistar male rats (11-week-old) reared at room temperature (21-25°C) on a 12:12 h light-dark cycle with ad libitum access to food and water. Under isoflurane anaesthesia, isometric contractions of the TA muscle of the rat right leg were induced by skin electrode stimulation using a surface electrode. Protein expression was measured in rat TA muscle before and 12 hours after exercise using a Q Exactive Plus Hybrid Quadrupole-Orbitrap mass spectrometer (Thermo Fisher Scientific).
2024-11-20 | PXD056315 | JPOST Repository
Project description:Exercise is a fundamental component of human health that is associated with greater life expectancy and reduced risk of chronic diseases. While the beneficial effects of endurance exercise on human health are well established, the molecular mechanisms responsible for these observations remain unclear. Endurance exercise reduces the accumulation of mitochondrial DNA (mtDNA) mutations, alleviates multisystem pathology, and increases the lifespan of the mtDNA mutator mouse model of aging, in which the proof-reading capacity of mitochondrial polymerase gamma (POLG1) is deficient. Clearly, exercise recruited a POLG1-independent mtDNA repair pathway to induce these adaptations, a novel finding as POLG1 is canonically considered to be the sole mtDNA repair enzyme. Here we investigate the identity of this pathway, and show that endurance exercise prevents mitochondrial oxidative damage, attenuates telomere erosion, and mitigates cellular senescence and apoptosis in mtDNA mutator mice. Unexpectedly, we observe translocation of tumour suppressor protein p53 to mitochondria in response to endurance exercise that facilitates mtDNA mutation repair. Indeed, endurance exercise failed to prevent mtDNA mutations, induce mitochondrial biogenesis, preserve mitochondrial morphology, reverse sarcopenia, and mitigate premature mortality in mtDNA mutator mice with muscle-specific deletion of p53. Our data establish an exciting new role for p53 in exercise-mediated maintenance of the mtDNA genome, and presents mitochondrially-targeted p53 as a novel therapeutic modality for aging-associated diseases of mitochondrial etiology. Microarray analysis of gene expression from skeletal muscle (quadriceps femoris) from Mus musculus. N=23 samples per treatment were analysed for whole transcriptiome gene expression profile using NimbleGen Arrays. The treatment groups included wild-type C57Bl/6J mice as the control group, then two treatment groups which both contained homozygous knock-in mtDNA mutator mice (PolG; PolgAD257A/D257A). Once group of these heterozygous knock out mice received regular endurance exercise sessions while the other group remained sedentraty for 6 months. The control group specimens were wild-type litter mates to the transgenic knockout mice.
2015-12-11 | E-GEOD-75869 | biostudies-arrayexpress
Project description:Mitochondria were isolated from skeletal muscle and the remaining tissue fraction was collected to identify RNA enriched in mitochondria.
2024-03-15 | GSE235762 | GEO
Project description:To investigate microRNAs related to mitochondria biogenesis in skeletal muscle, microRNA expressions during skeletal muscle differentiation and exercise were analyzed in vivo and in vitro. Murine skeletal muscle cell (C2C12) were assigned to undifferentiated, differentiated, and passively stretched (exercise mimicked). C57BL/6S mice were assigned to resting, acute exercise (1day), and chronic exercise (7days). Low molecular weight RNA (< 200 nucleotides) was isolated from C2C12 cell or tibialis anterior muscle of mice and hybridized to Ncode microRNA microarrays. The experiment was performed using a loop design for the data analysis.
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