ArticlePLoS biology2018
H3K36 trimethylation mediated by SETD2 regulates the fate of bone marrow mesenchymal stem cells.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 94 citations in OpenAlex.
- SCFSignal transduction and targeted therapy · 2026Article
- Cryptic transcription in aging.iScience · 2026Review
- Integrated epigenetic networks in aging: from histone to RNA modifications.Journal of translational medicine · 2026Review
- Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Research Hotspots and Emerging Trends in Osteoporosis Epigenetics.Genetics research · 2026Article
- Histone modifications: Unveiling the epigenetic enigma of degenerative skeletal diseases.Journal of orthopaedic translation · 2025Review
- Transcript diversity in aging: cryptic transcription and splicing.Medical review (2021) · 2025Review
- Evaluation of the osteogenic effect of Naringin-enhanced bmscs/cpc composite for alveolar ridge preservation and tooth extraction wound healing in beagle dogs.BMC oral health · 2025Article
- H3K36me3 modification by SETD2 is essential for Col11a2 and Sema3e transcription to maintain dentinogenesis in mice.Development (Cambridge, England) · 2025Article
- Review
- Molecular pathological insights into tumorigenesis and progression of giant cell tumor of bone.Journal of bone oncology · 2025Review
- Bioinformatics screening and clinical validation of CircRNA and related miRNA in male osteoporosis.BMC musculoskeletal disorders · 2025Article
- The Dynamics of Histone Modifications during Mammalian Zygotic Genome Activation.International journal of molecular sciences · 2024Review
- H3K36 methyltransferase NSD1 protects against osteoarthritis through regulating chondrocyte differentiation and cartilage homeostasis.Cell death and differentiation · 2024Article
- Epigenetic regulation of mesenchymal stem cell aging through histone modifications.Genes & diseases · 2023Review
- Histone methyltransferase SETD2 inhibits M1 macrophage polarization and glycolysis by suppressing HIF-1α in sepsis-induced acute lung injury.Medical microbiology and immunology · 2023Article
- Methylation across the central dogma in health and diseases: new therapeutic strategies.Signal transduction and targeted therapy · 2023Review
- Dysregulation of histone modifications in bone marrow mesenchymal stem cells during skeletal ageing: roles and therapeutic prospects.Stem cell research & therapy · 2023Review
- Impact of Environmental and Epigenetic Changes on Mesenchymal Stem Cells during Aging.International journal of molecular sciences · 2023Review
- Expression and significance of histone methyltransferase SET domain containing 2 with histone H3 lysine 36 trimethylation in mouse hepatic oval cells differentiated into bile duct epithelial cellsMolecular medicine reports · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During the aging process, bone marrow mesenchymal stem cells (BMSCs) exhibit declined osteogenesis accompanied by excess adipogenesis, which will lead to osteoporosis. Here, we report that the H3 lysine 36 trimethylation (H3K36me3), catalyzed by histone methyltransferase SET-domain-containing 2 (SETD2), regulates lineage commitment of BMSCs. Deletion of Setd2 in mouse bone marrow mesenchymal stem cells (mBMSCs), through conditional Cre expression driven by Prx1 promoter, resulted in bone loss and marrow adiposity. Loss of Setd2 in BMSCs in vitro facilitated differentiation propensity to adipocytes rather than to osteoblasts. Through conjoint analysis of RNA sequencing (RNA-seq) and chromatin immunoprecipitation sequencing (ChIP-seq) data, we identified a SETD2 functional target gene, Lbp, on which H3K36me3 was enriched, and its expression was affected by Setd2 deficiency. Furthermore, overexpression of lipopolysaccharide-binding protein (LBP) could partially rescue the lack of osteogenesis and enhanced adipogenesis resulting from the absence of Setd2 in BMSCs. Further mechanistic studies demonstrated that the trimethylation level of H3K36 could regulate Lbp transcriptional initiation and elongation. These findings suggest that H3K36me3 mediated by SETD2 could regulate the cell fate of mesenchymal stem cells (MSCs) in vitro and in vivo, indicating that the regulation of H3K36me3 level by targeting SETD2 and/or the administration of downstream LBP may represent a potential therapeutic way for new treatment in metabolic bone diseases, such as osteoporosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.