ArticleThe Journal of biological chemistry2012
The increase in O-linked N-acetylglucosamine protein modification stimulates chondrogenic differentiation both in vitro and in vivo.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 100 citations in OpenAlex.
- TGFBI Maintains Fibrocartilage Homeostasis by Restraining O-GlcNAcylation to Inactivate and Destabilize ADAMTS16 in Temporomandibular Joint Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Activation of farnesoid X receptor upregulates binding immunoglobulin protein expression and alleviates diabetic nephropathy.World journal of diabetes · 2025Article
- Impact of intra-articular high-concentration hyaluronic acid administration on the innate immune response in experimental knee osteoarthritis.BMC musculoskeletal disorders · 2025Article
- FHL2 deteriorates IL-1β induced inflammation, apoptosis, and extracellular matrix degradation in chondrocyte-like ATDC5 cells by mTOR and NF-ĸB pathways.BMC musculoskeletal disorders · 2025Article
- O-GlcNAcylation: Sagacious Orchestrator of Bone-, Joint-, and Spine-Related Diseases.Journal of proteome research · 2025Review
- Regulation of senescence-associated secretory phenotypes in osteoarthritis by cytosolic UDP-GlcNAc retention and O-GlcNAcylation.Nature communications · 2025Article
- FBXO31-mediated ubiquitination of OGT maintains O-GlcNAcylation homeostasis to restrain endometrial malignancy.Nature communications · 2025Article
- ER-resident proteins are key players in cartilage and bone homeostasis.Frontiers in cell and developmental biology · 2025Review
- Thiamet-G facilitates reparative dentin formation via modulating O-GlcNAcylation and inflammation.Frontiers in physiology · 2025Article
- An Efficient and Accessible Hectogram-Scale Synthesis for the Selective O-GlcNAcase Inhibitor Thiamet-G.ACS omega · 2024Article
- O-GlcNAcylation: roles and potential therapeutic target for bone pathophysiology.Cell communication and signaling : CCS · 2024Review
- Magnesium and Vascular Calcification in Chronic Kidney Disease: Current Insights.International journal of molecular sciences · 2024Review
- O-GlcNAc transferase regulates collagen deposition and fibrosis resolution in idiopathic pulmonary fibrosis.Frontiers in immunology · 2024Article
- The role of O-GlcNAcylation in bone metabolic diseases.Frontiers in physiology · 2024Review
- Age-related elevation of O-GlcNAc causes meiotic arrest in male mice.Cell death discovery · 2023Article
- The role of O-GlcNAcylation in development.Development (Cambridge, England) · 2023Article
- O-GlcNAc glycosylation orchestrates fate decision and niche function of bone marrow stromal progenitors.eLife · 2023Article
- Bioinformatic analysis reveals potential relationship between chondrocyte senescence and protein glycosylation in osteoarthritis pathogenesis.Frontiers in endocrinology · 2023Article
- Article
- A Connecting Link between Hyaluronan Synthase 3-Mediated Hyaluronan Production and Epidermal Function.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Insulin is an inducer of chondrocyte hypertrophy and growth plate chondrogenesis, although the specific molecular mechanisms behind these effects are mostly unknown. Our aim was to investigate whether insulin-induced chondrocyte hypertrophy occurs through a modification in the amount of O-linked N-acetylglucosamine (O-GlcNAc)-modified proteins and in the expression of the key enzymes of this pathway, O-GlcNAc transferase and O-GlcNAcase (OGA). We also studied if O-GlcNAc accumulation per se, induced by an OGA inhibitor, was able to induce pre-hypertrophic chondrocyte differentiation both in vitro and in vivo. Insulin-induced differentiation of ATDC5 pre-chondrocytes occurred alongside a gradual increase in the accumulation of O-GlcNac-modified proteins (O-GlcNAcylated proteins), as well as an increase in the expression of O-GlcNAc transferase and OGA. In the absence of insulin, O-GlcNAc accumulation induced by thiamet-G, a specific OGA inhibitor, was able to increase the gene expression of differentiation markers, as well as the activity of MMP-2 and -9. Thiamet-G also activated pERK, p-JNK, and p-p38 and the O-GlcNAcylation of Akt. Thiamet-G administration to C57/bl mice induced a significant expansion in the growth plate height and in the hypertrophic zone height. Therefore, our results show that O-GlcNAc glycosylation has chondromodulating activity.
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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.