ArticleJournal of cellular physiology2008
ESE-1 is a potent repressor of type II collagen gene (COL2A1) transcription in human chondrocytes.
Article in Journal of cellular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 59 citations in OpenAlex.
- E74-like ETS transcription factor 3 expression and regulation in human intervertebral disc.JOR spine · 2025Article
- Elf3 deficiency during zebrafish development alters extracellular matrix organization and disrupts tissue morphogenesis.PloS one · 2022Article
- Conditioned medium of IGF1-induced synovial membrane mesenchymal stem cells increases chondrogenic and chondroprotective markers in chondrocyte inflammation.Bioscience reports · 2021Article
- Runx2 plays a central role in Osteoarthritis development.Journal of orthopaedic translation · 2020Review
- Specific, Sensitive, and Stable Reporting of Human Mesenchymal Stromal Cell Chondrogenesis.Tissue engineering. Part C, Methods · 2019Article
- Elf3 Contributes to Cartilage Degradation in vivo in a Surgical Model of Post-Traumatic Osteoarthritis.Scientific reports · 2018Article
- CRISPR/Cas9 Editing of Murine Induced Pluripotent Stem Cells for Engineering Inflammation-Resistant Tissues.Arthritis & rheumatology (Hoboken, N.J.) · 2017Article
- ELF3 modulates type II collagen gene (COL2A1) transcription in chondrocytes by inhibiting SOX9-CBP/p300-driven histone acetyltransferase activity.Connective tissue research · 2017Article
- E74-like factor 3 and nuclear factor-κB regulate lipocalin-2 expression in chondrocytes.The Journal of physiology · 2016Article
- Blockade of Ets-1 attenuates epidermal growth factor-dependent collagen loss in human carotid plaque smooth muscle cells.American journal of physiology. Heart and circulatory physiology · 2015Article
- Comparative genomic profiling of synovium versus skin lesions in psoriatic arthritis.Arthritis & rheumatology (Hoboken, N.J.) · 2015Article
- Review
- New developments in the treatment of osteoarthritis - focus on biologic agents.Open access rheumatology : research and reviews · 2015Review
- Signaling pathways in cartilage repair.International journal of molecular sciences · 2014Review
- CCAAT/enhancer-binding protein β regulates the repression of type II collagen expression during the differentiation from proliferative to hypertrophic chondrocytes.The Journal of biological chemistry · 2014Article
- Epithelium-Specific ETS (ESE)-1 upregulated GP73 expression in hepatocellular carcinoma cells.Cell & bioscience · 2014Article
- Regulated transcription of human matrix metalloproteinase 13 (MMP13) and interleukin-1β (IL1B) genes in chondrocytes depends on methylation of specific proximal promoter CpG sites.The Journal of biological chemistry · 2013Article
- Article
- SOX9 and myocardin counteract each other in regulating vascular smooth muscle cell differentiation.Biochemical and biophysical research communications · 2012Article
- E74-like factor 3 (ELF3) impacts on matrix metalloproteinase 13 (MMP13) transcriptional control in articular chondrocytes under proinflammatory stress.The Journal of biological chemistry · 2012Article
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
The epithelium-specific ETS (ESE)-1 transcription factor is induced in chondrocytes by interleukin-1beta (IL-1beta). We reported previously that early activation of EGR-1 by IL-1beta results in suppression of the proximal COL2A1 promoter activity by displacement of Sp1 from GC boxes. Here we report that ESE-1 is a potent transcriptional suppressor of COL2A1 promoter activity in chondrocytes and accounts for the sustained, NF-kappaB-dependent inhibition by IL-1beta. Of the ETS factors tested, this response was specific to ESE-1, since ESE-3, which was also induced by IL-1beta, suppressed COL2A1 promoter activity only weakly. In contrast, overexpression of ETS-1 increased COL2A1 promoter activity and blocked the inhibition by IL-1beta. These responses to ESE-1 and ETS-1 were confirmed using siRNA-ESE1 and siRNA-ETS1. In transient cotransfections, the inhibitory responses to ESE-1 and IL-1beta colocalized in the -577/-132 bp promoter region, ESE-1 bound specifically to tandem ETS sites at -403/-381 bp, and IL-1-induced binding of ESE-1 to the COL2A1 promoter was confirmed in vivo by ChIP. Our results indicate that ESE-1 serves a potent repressor function by interacting with at least two sites in the COL2A1 promoter. However, the endogenous response may depend upon the balance of other ETS factors such as ETS-1, and other IL-1-induced factors, including EGR-1 at any given time. Intracellular ESE-1 staining in chondrocytes in cartilage from patients with osteoarthritis (OA), but not in normal cartilage, further suggests a fundamental role for ESE-1 in cartilage degeneration and suppression of repair.
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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.