Trichostatin A-Induced H3K9ac Hyperacetylation Selectively Enriches Promoters in Adipogenic Human Periodontal Ligament Stem Cells
6 affiliations
- 1Facultad de Ingeniería Química, Universidad Autónoma de Yucatán, Mérida 97203, Mexico
- 2Laboratorio de Células Troncales, Facultad de Odontología, Universidad Autónoma de Yucatán, Mérida 97000, Mexico
- 3Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados-Sede Sur, Ciudad de México 07360, Mexico
- 4Centro de Investigación sobre el Envejecimiento, Centro de Investigación y de Estudios Avanzados del I.P.N-Sede Sur, Ciudad de México 07360, Mexico
- 5Laboratorio de Bioquímica y Genética Molecular, Facultad de Química, Universidad Autónoma de Yucatán, Calle 43 s/n x 96 Paseo de las Fuentes y 40 Col. Inalámbrica, Mérida 97069, Mexico
- 6SECIHTI-Facultad de Ingeniería Química, Universidad Autónoma de Yucatán, Mérida 97203, Mexico
Abstract
Adipogenesis is regulated by histone modifications associated with chromatin accessibility. These modifications include histone H3 lysine 9 acetylation (H3K9ac), a mark linked to transcriptional activation. Its dynamics are governed by histone acetyltransferases and histone deacetylases (HDACs). Although trichostatin A (TSA) induces global hyperacetylation, its association with the differential enrichment of H3K9ac at regulatory elements during adipogenesis in human cells remains unclear. Therefore, this study characterized the genomic distribution of TSA-induced H3K9ac enrichment in human periodontal ligament stem cells (hPDLSCs). To this end, hPDLSCs underwent adipogenic differentiation for 14 days following TSA pretreatment (100 nM, 72 h). Cell morphology, lipid droplet radius, and the nuclear distribution of H3K9ac and H3K9me2 were evaluated by immunofluorescence, while the genomic distribution of H3K9ac was assessed by ChIP-seq. Statistical significance was assessed using an unpaired two-tailed Student’s t-test (p < 0.05) and MACS3 peak calling (q = 0.001). TSA reduced the lipid droplet radius by 1.69-fold and increased the nuclear H3K9ac signal by 10.17-fold, while reducing H3K9me2 signal by 1.38-fold. Furthermore, 752 promoters exhibited greater H3K9ac enrichment under TSA treatment compared with 364 in the control, including genes associated with adipogenesis, such as PPARGC1B and AGPAT2, and chromatin remodeling genes SETD5 and KDM2A. Overall, these findings indicate that TSA alters the adipogenic phenotype and increases H3K9ac enrichment at promoters associated with metabolic and chromatin remodeling programs.
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BibTeX
@article{monterodeltoro2026trichostatin,
title = {{Trichostatin A-Induced H3K9ac Hyperacetylation Selectively Enriches Promoters in Adipogenic Human Periodontal Ligament Stem Cells}},
author = {Julio A. Montero-Del-Toro and Angelica A. Serralta-Interian and Monica Lamas and David Valle-García and Julio C. Torres-Romero and Beatriz A. Rodas-Junco},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219898},
url = {https://www.mdpi.com/1422-0067/27/21/9898},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Trichostatin A-Induced H3K9ac Hyperacetylation Selectively Enriches Promoters in Adipogenic Human Periodontal Ligament Stem Cells
AU - Julio A. Montero-Del-Toro
AU - Angelica A. Serralta-Interian
AU - Monica Lamas
AU - David Valle-García
AU - Julio C. Torres-Romero
AU - Beatriz A. Rodas-Junco
PY - 2026
DA - 2026/11/05
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219898
UR - https://www.mdpi.com/1422-0067/27/21/9898
AB - Adipogenesis is regulated by histone modifications associated with chromatin accessibility. These modifications include histone H3 lysine 9 acetylation (H3K9ac), a mark linked to transcriptional activation. Its dynamics are governed by histone acetyltransferases and histone deacetylases (HDACs). Although trichostatin A (TSA) induces global hyperacetylation, its association with the differential enrichment of H3K9ac at regulatory elements during adipogenesis in human cells remains unclear. Therefore, this study characterized the genomic distribution of TSA-induced H3K9ac enrichment in human periodontal ligament stem cells (hPDLSCs). To this end, hPDLSCs underwent adipogenic differentiation for 14 days following TSA pretreatment (100 nM, 72 h). Cell morphology, lipid droplet radius, and the nuclear distribution of H3K9ac and H3K9me2 were evaluated by immunofluorescence, while the genomic distribution of H3K9ac was assessed by ChIP-seq. Statistical significance was assessed using an unpaired two-tailed Student’s t-test (p < 0.05) and MACS3 peak calling (q = 0.001). TSA reduced the lipid droplet radius by 1.69-fold and increased the nuclear H3K9ac signal by 10.17-fold, while reducing H3K9me2 signal by 1.38-fold. Furthermore, 752 promoters exhibited greater H3K9ac enrichment under TSA treatment compared with 364 in the control, including genes associated with adipogenesis, such as PPARGC1B and AGPAT2, and chromatin remodeling genes SETD5 and KDM2A. Overall, these findings indicate that TSA alters the adipogenic phenotype and increases H3K9ac enrichment at promoters associated with metabolic and chromatin remodeling programs.
SN - 1422-0067
ER -