ArticleBone2016
MMP-13 is one of the critical mediators of the effect of HDAC4 deletion on the skeleton.
Article in Bone, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 28 citations in OpenAlex.
- miRNAs in secondary hyperparathyroidism: literature review.BMC nephrology · 2025Review
- LMK-235 suppresses osteoclastogenesis and promotes osteoblastogenesis by inhibiting HDAC4.Scientific reports · 2024Article
- Dynamic Alterations in Acetylation and Modulation of Histone Deacetylase Expression Evident in the Dentine-Pulp Complex during Dentinogenesis.International journal of molecular sciences · 2024Article
- The Reparative Function of MMP13 in Tertiary Reactionary Dentinogenesis after Tooth Injury.International journal of molecular sciences · 2024Article
- Differential effects of parathyroid hormone, parathyroid hormone-related protein, and abaloparatide on collagen 1 expression by mouse cementoblasts and mouse tooth root density.American journal of orthodontics and dentofacial orthopedics : official publication of the American Association of Orthodontists, its constituent societies, and the American Board of Orthodontics · 2023Article
- HDAC4 in cancer: A multitasking platform to drive not only epigenetic modifications.Frontiers in molecular biosciences · 2023Review
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency.Scientific reports · 2022Article
- 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
- The Level of Histone Deacetylase 4 is Associated with Aging Cartilage Degeneration and Chondrocyte Hypertrophy.Journal of inflammation research · 2022Article
- Article
- Histone deacetylase 4 deletion results in abnormal chondrocyte hypertrophy and premature ossification from collagen type 2α1‑expressing cells.Molecular medicine reports · 2020Article
- Antibiotic Treatment Prior to Injury Improves Post-Traumatic Osteoarthritis Outcomes in Mice.International journal of molecular sciences · 2020Article
- Recent Advances of Osterix Transcription Factor in Osteoblast Differentiation and Bone Formation.Frontiers in cell and developmental biology · 2020Review
- Histone Acetylation as a Regenerative Target in the Dentine-Pulp Complex.Frontiers in genetics · 2020Review
- Hepatic Osteodystrophy-Molecular Mechanisms Proposed to Favor Its Development.International journal of molecular sciences · 2019Review
- Loss of histone methyltransferase Ezh2 stimulates an osteogenic transcriptional program in chondrocytes but does not affect cartilage development.The Journal of biological chemistry · 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
- Parathyroid hormone-induced down-regulation of miR-532-5p for matrix metalloproteinase-13 expression in rat osteoblasts.Journal of cellular biochemistry · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Histone deacetylase 4 (Hdac4) regulates chondrocyte hypertrophy. Hdac4(-/-) mice are runted in size and do not survive to weaning. This phenotype is primarily due to the acceleration of onset of chondrocyte hypertrophy and, as a consequence, inappropriate endochondral mineralization. Previously, we reported that Hdac4 is a repressor of matrix metalloproteinase-13 (Mmp13) transcription, and the absence of Hdac4 leads to increased expression of MMP-13 both in vitro (osteoblastic cells) and in vivo (hypertrophic chondrocytes and trabecular osteoblasts). MMP-13 is thought to be involved in endochondral ossification and bone remodeling. To identify whether the phenotype of Hdac4(-/-) mice is due to up-regulation of MMP-13, we generated Hdac4/Mmp13 double knockout mice and determined the ability of deletion of MMP-13 to rescue the Hdac4(-/-) mouse phenotype. Mmp13(-/-) mice have normal body size. Hdac4(-/-)/Mmp13(-/-) double knockout mice are significantly heavier and larger than Hdac4(-/-) mice, they survive longer, and they recover the thickness of their growth plate zones. In Hdac4(-/-)/Mmp13(-/-) double knockout mice, alkaline phosphatase (ALP) expression and TRAP-positive osteoclasts were restored (together with an increase in Mmp9 expression) but osteocalcin (OCN) was not. Micro-CT analysis of the tibiae revealed that Hdac4(-/-) mice have significantly decreased cortical bone area compared with the wild type mice. In addition, the bone architectural parameter, bone porosity, was significantly decreased in Hdac4(-/-) mice. Hdac4(-/-)/Mmp13(-/-) double knockout mice recover these cortical parameters. Likewise, Hdac4(-/-) mice exhibit significantly increased Tb.Th and bone mineral density (BMD) while the Hdac4(-/-)/Mmp13(-/-) mice significantly recovered these parameters toward normal for this age. Taken together, our findings indicate that the phenotype seen in the Hdac4(-/-) mice is partially derived from elevation in MMP-13 and may be due to a bone remodeling disorder caused by overexpression of this enzyme.
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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.