ArticleThe Journal of biological chemistry2010
HDAC4 represses matrix metalloproteinase-13 transcription in osteoblastic cells, and parathyroid hormone controls this repression.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 86 citations in OpenAlex.
- Review
- Review
- The Reparative Function of MMP13 in Tertiary Reactionary Dentinogenesis after Tooth Injury.International journal of molecular sciences · 2024Article
- The role of magnesium in the pathogenesis of osteoporosis.Frontiers in endocrinology · 2024Review
- Pathophysiology of bone disease in chronic kidney disease: from basics to renal osteodystrophy and osteoporosis.Frontiers in physiology · 2023Review
- The Critical Role of MMP13 in Regulating Tooth Development and Reactionary Dentinogenesis Repair Through the Wnt Signaling Pathway.Frontiers in cell and developmental biology · 2022Article
- Effects of 4-Hexylresorcinol on Craniofacial Growth in Rats.International journal of molecular sciences · 2021Article
- MiR-218 affects hypertrophic differentiation of human mesenchymal stromal cells during chondrogenesis via targeting RUNX2, MEF2C, and COL10A1.Stem cell research & therapy · 2020Article
- Mechanical strain-mediated reduction in RANKL expression is associated with RUNX2 and BRD2.Gene: X · 2020Article
- The role of histone deacetylase 4 during chondrocyte hypertrophy and endochondral bone development.Bone & joint research · 2020Review
- Hepatic Osteodystrophy-Molecular Mechanisms Proposed to Favor Its Development.International journal of molecular sciences · 2019Review
- Systems biology reveals how altered TGFβ signalling with age reduces protection against pro-inflammatory stimuli.PLoS computational biology · 2019Article
- Parathyroid hormone(1-34) and its analogs differentially modulate osteoblasticThe Journal of biological chemistry · 2018Article
- Syringic acid, a phenolic acid, promotes osteoblast differentiation by stimulation of Runx2 expression and targeting of Smad7 by miR-21 in mouse mesenchymal stem cells.Journal of cell communication and signaling · 2018Article
- Regulation of Bone Remodeling by Parathyroid Hormone.Cold Spring Harbor perspectives in medicine · 2018Review
- Parathyroid hormone-induced down-regulation of miR-532-5p for matrix metalloproteinase-13 expression in rat osteoblasts.Journal of cellular biochemistry · 2018Article
- The Deletion of Hdac4 in Mouse Osteoblasts Influences Both Catabolic and Anabolic Effects in Bone.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2018Article
- MEF2C Interacts With c-FOS in PTH-Stimulated Mmp13 Gene Expression in Osteoblastic Cells.Endocrinology · 2017Article
- The Good the Bad and the Ugly of Glycosaminoglycans in Tissue Engineering Applications.Pharmaceuticals (Basel, Switzerland) · 2017Review
- miR-365 Ameliorates Dexamethasone-Induced Suppression of Osteogenesis in MC3T3-E1 Cells by Targeting HDAC4.International journal of molecular sciences · 2017Article
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Parathyroid hormone (PTH) is a hormone regulating bone remodeling through its actions on both bone formation and bone resorption. Previously we reported that PTH induces matrix metalloproteinase-13 (MMP-13) transcription in osteoblastic cells. Here, we show that histone deacetylase 4 (HDAC4) interacts with Runx2, binds the MMP-13 promoter, and suppresses MMP-13 gene transcription in the rat osteoblastic cell line, UMR 106-01. PTH induces the rapid cAMP-dependent protein kinase-dependent release of HDAC4 from the MMP-13 promoter and subsequent transcription of MMP-13. Knock-out of HDAC4 either by siRNA in vitro or by gene deletion in vivo leads to an increase in MMP-13 expression, and overexpression of HDAC4 decreases the PTH induction of MMP-13. All of these observations indicate that HDAC4 represses MMP-13 gene transcription in bone. Moreover, PTH stimulates HDAC4 gene expression and enzymatic activity at times corresponding to the reassociation of HDAC4 with the MMP-13 promoter and a decline in its transcription. Thus, HDAC4 is a basal repressor of MMP-13 transcription, and PTH regulates HDAC4 to control MMP-13 promoter activity. These data identify a novel and discrete mechanism of regulating HDAC4 levels and, subsequently, gene expression.
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