Physical Activity and DNA Methylation in Humans

Światowy, Witold Józef; Drzewiecka, Hanna; Kliber, Michalina; Sąsiadek, Maria M.; Karpiński, Paweł; Pławski, Andrzej; Jagodzińśki, Paweł P.

doi:10.3390/ijms222312989

Cited by 44 publications

(20 citation statements)

References 78 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Research interest into how exercise affects genome-wide skeletal muscle DNA methylation has increased in recent years, and multiple associated reviews have been published [25,[44][45][46]. Barres et al [19] were the first to report that the hypomethylation of various metabolic genes occurs in skeletal muscle following a single high-intensity aerobic exercise session in humans, and that these events corresponded with an alteration in the mRNA expression levels of these genes.…”

Section: Insert Table 2 Here Discussionmentioning

confidence: 99%

Skeletal muscle DNA methylation and mRNA responses to a bout of higher versus lower load resistance exercise in previously trained men

Sexton

Godwin

McIntosh

et al. 2022

Preprint

View full text Add to dashboard Cite

We sought to determine the skeletal muscle genome-wide DNA methylation and mRNA responses to one bout of lower-load (LL) versus higher-load (HL) resistance exercise. Trained college-aged males (n=11, 23+/-4 years old, 4+/-3 years self-reported training) performed LL or HL bouts to failure separated by one week. The HL bout (i.e., 80 Fail) consisted of four sets of back squats and four sets of leg extensions to failure using 80% of participants estimated one-repetition maximum (i.e., est. 1-RM). The LL bout (i.e., 30 Fail) implemented the same paradigm with 30% of est. 1-RM. Vastus lateralis muscle biopsies were collected before, 3 hours, and 6 hours after each bout. Muscle DNA and RNA were batch-isolated and analyzed using the 850k Illumina MethylationEPIC array and Clariom S mRNA microarray, respectively. Performed repetitions were significantly greater during the 30 Fail versus 80 Fail (p<0.001), although total training volume (sets x reps x load) was not significantly different between bouts (p=0.571). Regardless of bout, more CpG site methylation changes were observed at 3- versus 6-hours post exercise (239,951 versus 12,419, respectively; p<0.01), and nuclear global ten-eleven translocation (TET) activity, but not global DNA methyltransferase activity, increased 3- and 6-hours following exercise regardless of bout. The percentage of genes significantly altered at the mRNA level that demonstrated opposite DNA methylation patterns was greater 3- versus 6-hours following exercise (~75% versus ~15%, respectively). Moreover, high percentages of genes that were up- or downregulated 6 hours following exercise also demonstrated significantly inversed DNA methylation patterns across one or more CpG sites 3 hours following exercise (65% and 82%, respectively). While 30 Fail decreased DNA methylation across various promoter regions versus 80 Fail, transcriptome-wide mRNA and bioinformatics indicated that gene expression signatures were largely similar between bouts. Bioinformatics overlay of DNA methylation and mRNA expression data indicated that genes related to Focal adhesion, MAPK signaling, and PI3K-Akt signaling were significantly affected at the 3- and 6-hour time points, and again this was regardless of bout. In conclusion, extensive molecular profiling suggests that post-exercise alterations in the skeletal muscle DNA methylome and mRNA transcriptome elicited by LL and HL training bouts to failure are largely similar, and this could be related to equal volumes performed between bouts.

show abstract

Section: Insert Table 2 Here Discussionmentioning

confidence: 99%

Skeletal muscle DNA methylation and mRNA responses to a bout of higher versus lower load resistance exercise in previously trained men

Sexton

Godwin

McIntosh

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…It seems that the sedentary lifestyle is correlated with an unfavorable epigenome. Exercise has been shown to increase DNA methylation in peripheral blood cells and alter histone acetylation (lysine 36-H3 acetylation) [ 17 , 118 , 119 ]. Other studies suggest that exercise induces both dynamic changes in H4 deacetylation/loss of promoter methylation and transient changes in miRNA expression profiles [ 17 , 118 ].…”

Section: Discussion and Future Challengesmentioning

confidence: 99%

“…Exercise has been shown to increase DNA methylation in peripheral blood cells and alter histone acetylation (lysine 36-H3 acetylation) [ 17 , 118 , 119 ]. Other studies suggest that exercise induces both dynamic changes in H4 deacetylation/loss of promoter methylation and transient changes in miRNA expression profiles [ 17 , 118 ]. Identifying the dynamics of epigenetic regulation could allow for effective therapeutic interventions involving the direct modulation of gene expression by modifying environmental factors [ 17 , 119 , 120 ].…”

Section: Discussion and Future Challengesmentioning

confidence: 99%

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Butnariu

Gorduza

Florea

et al. 2022

IJMS

View full text Add to dashboard Cite

Lower extremity artery disease (LEAD), caused by atherosclerotic obstruction of the arteries of the lower limb extremities, has exhibited an increase in mortality and morbidity worldwide. The phenotypic variability of LEAD is correlated with its complex, multifactorial etiology. In addition to traditional risk factors, it has been shown that the interaction between genetic factors (epistasis) or between genes and the environment potentially have an independent role in the development and progression of LEAD. In recent years, progress has been made in identifying genetic variants associated with LEAD, by Genome-Wide Association Studies (GWAS), Whole Exome Sequencing (WES) studies, and epigenetic profiling. The aim of this review is to present the current knowledge about the genetic factors involved in the etiopathogenic mechanisms of LEAD, as well as possible directions for future research. We analyzed data from the literature, starting with candidate gene-based association studies, and then continuing with extensive association studies, such as GWAS and WES. The results of these studies showed that the genetic architecture of LEAD is extremely heterogeneous. In the future, the identification of new genetic factors will allow for the development of targeted molecular therapies, and the use of polygenic risk scores (PRS) to identify individuals at an increased risk of LEAD will allow for early prophylactic measures and personalized therapy to improve their prognosis.

show abstract

“…Additionally, in the present study, both HbSS and HbSC groups showed statistically significant DMPs distribution in the regions related to CpG Island with hypermethylation at CpG Island and S_Shore regions, and hypomethylation at Open Sea region. Approximately 60–70% of the genes in the human genome present CpGs Island, especially in promoter regions, and its methylation is closely associated to gene silencing [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Epigenetic analysis in placentas from sickle cell disease patients reveals a hypermethylation profile

et al. 2022

View full text Add to dashboard Cite

Pregnancy in Sickle Cell Disease (SCD) women is associated to increased risk of clinical and obstetrical complications. Placentas from SCD pregnancies can present increased abnormal findings, which may lead to placental insufficiency, favoring adverse perinatal outcome. These placental abnormalities are well known and reported, however little is known about the molecular mechanisms, such as epigenetics. Thus, our aim was to evaluate the DNA methylation profile in placentas from women with SCD (HbSS and HbSC genotypes), compared to uncomplicated controls (HbAA). We included in this study 11 pregnant women with HbSS, 11 with HbSC and 21 with HbAA genotypes. Illumina Methylation EPIC BeadChip was used to assess the whole placental DNA methylation. Pyrosequencing was used for array data validation and qRT-PCR was applied for gene expression analysis. Our results showed high frequency of hypermethylated CpGs sites in HbSS and HbSC groups with 73.5% and 76.2% respectively, when compared with the control group. Differentially methylated regions (DMRs) also showed an increased hypermethylation status for the HbSS (89%) and HbSC (86%) groups, when compared with the control group methylation data. DMRs were selected for methylation validation (4 DMRs-HbSS and 3 DMRs the HbSC groups) and after analyses three were validated in the HbSS group, and none in the HbSC group. The gene expression analysis showed differential expression for the PTGFR (-2.97-fold) and GPR56 (3.0-fold) genes in the HbSS group, and for the SPOCK1 (-2.40-fold) and ADCY4 (1.80-fold) genes in the HbSC group. Taken together, these data strongly suggest that SCD (HbSS and HbSC genotypes) can alter placental DNA methylation and lead to gene expression changes. These changes possibly contribute to abnormal placental development and could impact in the clinical course, especially for the fetus, possibly leading to increased risk of abortion, fetal growth restriction (FGR), stillbirth, small for gestational age newborns and prematurity.

show abstract

Physical Activity and DNA Methylation in Humans

Cited by 44 publications

References 78 publications

Skeletal muscle DNA methylation and mRNA responses to a bout of higher versus lower load resistance exercise in previously trained men

Skeletal muscle DNA methylation and mRNA responses to a bout of higher versus lower load resistance exercise in previously trained men

The Genetic Architecture of the Etiology of Lower Extremity Peripheral Artery Disease: Current Knowledge and Future Challenges in the Era of Genomic Medicine

Epigenetic analysis in placentas from sickle cell disease patients reveals a hypermethylation profile

Contact Info

Product

Resources

About