CDNA microarray analysis of human skeletal muscle after eccentric exercise
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Douglas Mahoney
PROVIDER: E-GEOD-4249 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:We examined global mRNA expression using cDNA microarrays in skeletal muscle of humans before, and 3h and 48h after 300 maximal eccentric contractions. Keywords: Time course
2006-04-15 | GSE4249 | GEO
Project description:We examined global mRNA expression using cDNA microarrays in skeletal muscle of humans before, and 3h and 48h after a single bout of exhaustive endurance exercise (cycling). Keywords: Time course Healthy, non-trained university-aged subjects performed a single bout of exhaustive cycling. Skeletal muscle biopsies were taken from the vastus lateralis before, 3h and 48h after the exercise bout. Total RNA was extracted, amplified, reverse transcribed, and cDNA was analyzed on a custom made cDNA microarray. Four subjects were analyzed, and samples were not pooled between subjects (i.e. individual microarrays were used for baseline vs. 3H and baseline vs. 48h for EACH subject; repeated measures design).
2006-02-17 | E-GEOD-4247 | biostudies-arrayexpress
Project description:Full title: Eccentric exercise activates novel transcriptional regulation of hypertrophic signaling pathways not affected by hormone changes. Unaccustomed eccentric exercise damages muscle tissue stimulating mechanisms of recovery and remodeling that may be affected by cellular protection by the sex hormone 17β-estradiol (E2). Using cDNA microarrays, we screened for differences in mRNA expression caused by E2 and eccentric exercise. After randomly assignment to 8 days of either placebo (CON) or E2 (EXP), eighteen men performed 150 single-leg eccentric contractions. Muscle biopsies were collected at baseline (BL), following supplementation (PS), +3 hours (3H) and +48 hours (48H) after exercise. Serum E2 concentrations increased significantly with supplementation (P < 0.001) but did not affect microarray results. Exercise led to early transcriptional changes in striated muscle activator of Rho signaling (STARS), Rho family GTPase 3 (RND3), mitogen activated protein kinase (MAPK) regulation and the downstream transcription factor FOS. Targeted RT-PCR analysis identified concurrent induction of negative regulators of calcineurin signaling RCAN (P < 0.001) and HMOX1 (P = 0.009). Protein contents were elevated for RND3 at 3H (P = 0.02) and FOS at 48H (P < 0.05). These findings indicate that early RhoA and NFAT signaling and regulation are altered following exercise for muscle remodeling and repair, but are not affected by E2.
2009-12-16 | GSE19062 | GEO
Project description:Full title: Eccentric exercise activates novel transcriptional regulation of hypertrophic signaling pathways not affected by hormone changes. Unaccustomed eccentric exercise damages muscle tissue stimulating mechanisms of recovery and remodeling that may be affected by cellular protection by the sex hormone 17β-estradiol (E2). Using cDNA microarrays, we screened for differences in mRNA expression caused by E2 and eccentric exercise. After randomly assignment to 8 days of either placebo (CON) or E2 (EXP), eighteen men performed 150 single-leg eccentric contractions. Muscle biopsies were collected at baseline (BL), following supplementation (PS), +3 hours (3H) and +48 hours (48H) after exercise. Serum E2 concentrations increased significantly with supplementation (P < 0.001) but did not affect microarray results. Exercise led to early transcriptional changes in striated muscle activator of Rho signaling (STARS), Rho family GTPase 3 (RND3), mitogen activated protein kinase (MAPK) regulation and the downstream transcription factor FOS. Targeted RT-PCR analysis identified concurrent induction of negative regulators of calcineurin signaling RCAN (P < 0.001) and HMOX1 (P = 0.009). Protein contents were elevated for RND3 at 3H (P = 0.02) and FOS at 48H (P < 0.05). These findings indicate that early RhoA and NFAT signaling and regulation are altered following exercise for muscle remodeling and repair, but are not affected by E2. Eighteen young healthy men volunteered as participants in this study. All subjects were pre-screened to ensure that they were healthy, fit and had not regularly participated in resistance exercise in the preceding 6 months. Body composition was measured using dual energy x-ray absorptiometry (DEXA) scans (Hologic QDR 1000W, Waltham, MA). Thigh muscle cross-sectional area was calculated using anthropomorphic measurements of mid-thigh circumference and skinfold thickness. The subject demographics were (mean ± SD): age, 21 ± 2 y; height, 181 ± 5 cm; weight, 76.9 ± 12.8 kg. Subjects were assigned in a randomized, double-blind manner to either a control (CON, N=9) or experimental (EXP, N=9) group. CON subjects consumed 400 mg glucose polymer (Polycose; Abbott Laboratories, Ross Division, St. Laurent, Quebec, Canada) for 10 days. EXP subjects consumed ~300 mg glucose with 1 mg E2 (Estrace; Shire BioChem, Inc., St. Laurent, Quebec, Canada) for 2 days followed by 2 mg E2 for 8 days. On the morning of the ninth day, subjects reported to the laboratory and performed the exercise protocol. Supplementation continued until the day of the final biopsy and blood collection to maintain serum E2 concentrations throughout the collection protocol. Subjects in both groups were instructed to take one pill at the same time each day and return any unused pills. On the testing day, following a short warm-up (10 min of light cycling), subjects were seated in a Biodex isokinetic dynamometer (System 3, Biodex Medical Systems Inc., Ronkonkoma, NY) with their right leg strapped to a lever arm. The lever arm was programmed to extend their leg to 150º of flexion (where 180º is full extension) at a moderate speed (30º/s), then flex their leg to 90°of flexion at a faster speed (120°/s). During the flexion phase, subjects were instructed to attempt to maximally resist flexion of the knee (i.e. voluntary ‘maximal’ contraction) against the descending lever arm throughout the entire range of motion. The complete test consisted of 15 sets of 10 repetitions, each set separated by 1 minute of rest. Prior to each tissue collection, subjects abstained from any other form of physical exertion (within 72 h), avoided alcohol (within 48 h), ate their habitual diet (within 48 h), and abstained from caffeine (within 12 h). Each subject consumed a 350 Kcal defined formula diet (57% carbohydrates, 15% protein and 28% fat) two hours before each muscle biopsy and did not eat again until after the final biopsy of each session was taken. Muscle biopsies were taken from the vastus lateralis of the control (left) leg during the familiarization session (baseline, BL) and after 8 days of supplementation (post supplementation, PS) and the exercised (right) leg 3 hours (3H) and 48 hours (48H) after exercise, in anatomically distinct sites approximately 6 cm apart. Blood was drawn from the antecubital vein at the same collection times. Muscle and blood samples were processed and stored for future measurements.
2009-12-16 | E-GEOD-19062 | biostudies-arrayexpress
Project description:Eccentric exercise (ECC) can result in ultra-structural and histological damage to skeletal muscle. The damage incurred following ECC is typically followed by a subsequent regenerative and adaptive response. The specific mechanisms that drive this response, particularly in human muscle, are not well understood. The objective of this study was to characterize the early molecular response in skeletal muscle following ECC in humans. We used an Agilent whole human genome microarray to assess global gene expression in male subjects (N=35) at 3 hours post-100 eccentric contractions of the knee extensors. ANCOVA (age and BMI covariates) was used to compare mRNA expression between the ECC and non-exercised (CON) legs of each subject. Novel transcripts from IPA identified networks were confirmed with quantitative real-time (qRT)-PCR. qRT-PCR analysis of 3 of these transcripts (IkBα, TNFRSF1A and ICAM-1) confirmed changes observed in the microarray analysis. 35 male subjects performed an eccentric exercise protocol consisting of 100 maximal eccentric contrations of the knee extensors. 3 hours after the completion of the exercise regimen, a muscle biopsy was taken from the vastus lateralis of both legs. The non-exercised leg served as the control. Gene expresssion was analyzed using an ANCOVA, with covariates for age and BMI.
2010-10-04 | E-GEOD-23697 | biostudies-arrayexpress
Project description:We examined global mRNA expression using cDNA microarrays in skeletal muscle of humans before, and 3h and 48h after a single bout of exhaustive endurance exercise (cycling). Keywords: Time course
2006-02-17 | GSE4247 | GEO
Project description:The study explores how maximal-intensity contractions and rapamycin impact the proteome and phosphoproteome of mouse skeletal muscle.
2021-01-20 | MSV000086732 | MassIVE
Project description:H3S10ph cistromes after eccentric contractions of mouse skeletal muscles
| PRJNA586864 | ENA
Project description:Eccentric exercise (ECC) can result in ultra-structural and histological damage to skeletal muscle. The damage incurred following ECC is typically followed by a subsequent regenerative and adaptive response. The specific mechanisms that drive this response, particularly in human muscle, are not well understood. The objective of this study was to characterize the early molecular response in skeletal muscle following ECC in humans. We used an Agilent whole human genome microarray to assess global gene expression in male subjects (N=35) at 3 hours post-100 eccentric contractions of the knee extensors. ANCOVA (age and BMI covariates) was used to compare mRNA expression between the ECC and non-exercised (CON) legs of each subject. Novel transcripts from IPA identified networks were confirmed with quantitative real-time (qRT)-PCR. qRT-PCR analysis of 3 of these transcripts (IkBα, TNFRSF1A and ICAM-1) confirmed changes observed in the microarray analysis.
2010-10-04 | GSE23697 | GEO
Project description:Duchenne muscular dystrophy (DMD) is an X-linked recessive disease caused by deleterious mutations in the DMD gene, rendering non-functional forms or complete absence of the protein dystrophin. Eccentric contraction-induced force loss is the most robust and reproducible phenotype of dystrophin-deficient skeletal muscle, yet the molecular mechanisms underlying force loss remain obscure. To this end, we utilized the mdx mouse model of DMD, which displays extreme sensitivity to eccentric contractions. An existing mouse line from our lab that overexpresses cytoplasmic gamma-actin specifically in skeletal muscle (mdx/Actg1-TG) was shown to significantly protect mdx muscle against contraction-induced force loss. To understand the mechanism behind this protection, we performed iTRAQ proteomics on mdx/Actg1-TG tibialis anterior (TA) muscle versus non-transgenic littermate controls to identify differentially-expressed proteins that may afford protection upon gamma-actin overexpression.
2018-10-22 | PXD009680 | Pride