Stress fiber traction force reshapes chromatin accessibility and YAP binding to direct diverse transcriptional programs in mesenchymal stem cells
Lei J., Long Y., Liu X., Chu Z., Wei Q.
Laboratory Study, published in Mechanobiol Med (2026) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Mechanobiol Med (2026)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41858407
- PMCID
- PMC12995898
- DOI
- 10.1016/j.mbm.2026.100178
Abstract (original English)
Stress fiber-generated traction forces critically regulate mesenchymal stem cell (MSC) behavior, yet how mechanical cues are integrated across transcriptional programs remains unclear. Here, we attenuated actomyosin contractility in human MSCs and performed parallel Assay for Transposase-Accessible Chromatin with high-throughput sequencing (ATAC-seq), YAP-targeted Cleavage Under Targets and Tagmentation sequencing (CUT&Tag) and RNA-seq profiling. We show that reduced stress fiber traction force selectively reorganizes chromatin accessibility into coherent functional modules, resulting in diverse transcriptional programs. The mechanosensitive co-activator YAP functions as a parallel force-responsive regulatory layer coordinating with chromatin accessibility changes. Integration of chromatin accessibility, YAP occupancy, and transcriptomic profiles reveals pathway-specific regulatory responses, identifying focal adhesion and PI3K-Akt signaling as central mechanosensitive pathways coordinated across layers. Together, these findings establish a modular framework for force-dependent gene regulation, demonstrating how mechanical signals are integrated across epigenomic and transcriptional networks to shape MSC transcriptional programs.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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