DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice

Abstract Disuse muscle atrophy can result in downregulated gene expression vital to muscle integrity, yet the mechanisms driving this downregulation remain unclear. Epigenetic alterations regulate transcriptional potential, with repressive changes suppressing gene expression. This study explored epi...

Full description

Saved in:
Bibliographic Details
Main Authors: Junya Shimizu, Fuminori Kawano
Format: Article
Language:English
Published: Wiley 2025-04-01
Series:Physiological Reports
Subjects:
Online Access:https://doi.org/10.14814/phy2.70317
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850150748918120448
author Junya Shimizu
Fuminori Kawano
author_facet Junya Shimizu
Fuminori Kawano
author_sort Junya Shimizu
collection DOAJ
description Abstract Disuse muscle atrophy can result in downregulated gene expression vital to muscle integrity, yet the mechanisms driving this downregulation remain unclear. Epigenetic alterations regulate transcriptional potential, with repressive changes suppressing gene expression. This study explored epigenetic mechanisms of gene downregulation during disuse muscle atrophy. Male C57BL/6J mice underwent hindlimb suspension for 3 or 7 days. The vastus intermedius (VI) muscle was analyzed, showing unchanged mass on day 3, but on day 7, decreased mass and reduced fiber size were assessed via immunohistochemistry. Corresponding to this atrophy timing, qPCR analysis revealed nine downregulated genes on day 7, which were selected for epigenetic analysis; collectively, they showed no downregulation on day 3. Among the nine genes, methylated DNA immunoprecipitation revealed significantly elevated DNA methylation (hypermethylation) in the upstream regions of transcription start sites (TSS) on day 7, which overall negatively correlated with gene expression. Histone marks (H3K27me3, H3K4me3, H3.3, and total H3) were also assessed using chromatin immunoprecipitation, revealing that the repressive histone mark H3K27me3 increased in the regions on day 3 but decreased on day 7. These findings suggest that DNA hypermethylation in the upstream regions preceded by H3K27me3 enrichment contributes to the downregulation of gene expression during disuse muscle atrophy.
format Article
id doaj-art-a450358398df4cd78effa124676887e0
institution OA Journals
issn 2051-817X
language English
publishDate 2025-04-01
publisher Wiley
record_format Article
series Physiological Reports
spelling doaj-art-a450358398df4cd78effa124676887e02025-08-20T02:26:27ZengWileyPhysiological Reports2051-817X2025-04-01137n/an/a10.14814/phy2.70317DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male miceJunya Shimizu0Fuminori Kawano1Graduate School of Health Science Matsumoto University Nagano JapanGraduate School of Health Science Matsumoto University Nagano JapanAbstract Disuse muscle atrophy can result in downregulated gene expression vital to muscle integrity, yet the mechanisms driving this downregulation remain unclear. Epigenetic alterations regulate transcriptional potential, with repressive changes suppressing gene expression. This study explored epigenetic mechanisms of gene downregulation during disuse muscle atrophy. Male C57BL/6J mice underwent hindlimb suspension for 3 or 7 days. The vastus intermedius (VI) muscle was analyzed, showing unchanged mass on day 3, but on day 7, decreased mass and reduced fiber size were assessed via immunohistochemistry. Corresponding to this atrophy timing, qPCR analysis revealed nine downregulated genes on day 7, which were selected for epigenetic analysis; collectively, they showed no downregulation on day 3. Among the nine genes, methylated DNA immunoprecipitation revealed significantly elevated DNA methylation (hypermethylation) in the upstream regions of transcription start sites (TSS) on day 7, which overall negatively correlated with gene expression. Histone marks (H3K27me3, H3K4me3, H3.3, and total H3) were also assessed using chromatin immunoprecipitation, revealing that the repressive histone mark H3K27me3 increased in the regions on day 3 but decreased on day 7. These findings suggest that DNA hypermethylation in the upstream regions preceded by H3K27me3 enrichment contributes to the downregulation of gene expression during disuse muscle atrophy.https://doi.org/10.14814/phy2.70317disuse muscle atrophyDNA methylationepigenetic alterationsgene expressionH3K27me3
spellingShingle Junya Shimizu
Fuminori Kawano
DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
Physiological Reports
disuse muscle atrophy
DNA methylation
epigenetic alterations
gene expression
H3K27me3
title DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
title_full DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
title_fullStr DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
title_full_unstemmed DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
title_short DNA hypermethylation preceded by H3K27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
title_sort dna hypermethylation preceded by h3k27 trimethylation is linked to downregulation of gene expression in disuse muscle atrophy in male mice
topic disuse muscle atrophy
DNA methylation
epigenetic alterations
gene expression
H3K27me3
url https://doi.org/10.14814/phy2.70317
work_keys_str_mv AT junyashimizu dnahypermethylationprecededbyh3k27trimethylationislinkedtodownregulationofgeneexpressionindisusemuscleatrophyinmalemice
AT fuminorikawano dnahypermethylationprecededbyh3k27trimethylationislinkedtodownregulationofgeneexpressionindisusemuscleatrophyinmalemice