ArticleThe ocular surface2024
HDAC1/2 and HDAC3 play distinct roles in controlling adult Meibomian gland homeostasis.
Article in The ocular surface, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- Epigenetic Regulation of Sebaceous and Meibomian Glands: From Development to Disease.Biomedicines · 2026Review
- KRT6A and KRT17 Mark Distinct Stem Cell Populations in the Adult Palpebral Conjunctiva and Meibomian Gland.Cells · 2025Article
- Disruption of Krox20-Notch1 signaling blocks meibomian gland development and homeostasis leading to dry eye disease.Nature communications · 2025Article
- Identification of Meibomian gland stem cell populations and mechanisms of aging.Nature communications · 2025Article
- Identification of Meibomian gland stem cell populations and mechanisms of aging.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
purposeTo investigate the roles of HDAC1/2 and HDAC3 in adult Meibomian gland (MG) homeostasis.
methodsHDAC1/2 or HDAC3 were inducibly deleted in MG epithelial cells of adult mice. The morphology of MG was examined. Proliferation, apoptosis, and expression of MG acinus and duct marker genes, meibocyte differentiation genes, and HDAC target genes, were analyzed via immunofluorescence, TUNEL assay, and RNA in situ hybridization.
resultsCo-deletion of HDAC1/2 in MG epithelium caused gradual loss of acini and formation of cyst-like structures in the central duct. These phenotypes required homozygous deletion of both HDAC1 and HDAC2, indicating that they function redundantly in the adult MG. Short-term deletion of HDAC1/2 in MG epithelium had little effect on meibocyte maturation but caused decreased proliferation of acinar basal cells, excessive DNA damage, ectopic apoptosis, and increased p53 acetylation and p16 expression in the MG. By contrast, HDAC3 deletion in MG epithelium caused dilation of central duct, atrophy of acini, defective meibocyte maturation, increased acinar basal cell proliferation, and ectopic apoptosis and DNA damage. Levels of p53 acetylation and p21 expression were elevated in HDAC3-deficient MGs, while the expression of the differentiation regulator PPARγ and the differentiation markers PLIN2 and FASN was downregulated.
conclusionsHDAC1 and HDAC2 function redundantly in adult Meibomian gland epithelial progenitor cells and are essential for their proliferation and survival, but not for acinar differentiation, while HDAC3 is required to limit acinar progenitor cell proliferation and permit differentiation. HDAC1/2 and HDAC3 have partially overlapping roles in maintaining survival of MG cells.
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