ArticleJournal of molecular medicine (Berlin, Germany)2014
Up-regulation of type II collagen gene by 17β-estradiol in articular chondrocytes involves Sp1/3, Sox-9, and estrogen receptor α.
Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 35 citations in OpenAlex.
- Estrogen deficiency as a common driver and integrative mechanism in osteoporosis‑osteoarthritis comorbidity (Review).Molecular medicine reports · 2026Review
- Therapeutic potential of SOX family transcription factors in osteoarthritis.Annals of medicine · 2025Review
- Sex-dependent variation in cartilage adaptation: from degeneration to regeneration.Biology of sex differences · 2023Review
- Timing Expression of miR203a-3p during OA Disease: Preliminary In Vitro Evidence.International journal of molecular sciences · 2023Article
- In vitro study to identify ligand-independent function of estrogen receptor-α in suppressing DNA damage-induced chondrocyte senescence.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Article
- Estrogenic impregnation alters pain expression: analysis through functional neuropeptidomics in a surgical rat model of osteoarthritis.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Anti-Inflammatory Mechanisms of Fucoidans to Treat Inflammatory Diseases: A Review.Marine drugs · 2021Review
- Up-regulation of sex-determining region Y-box 9 (SOX9) in growth hormone-secreting pituitary adenomas.BMC endocrine disorders · 2021Article
- How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights.International journal of molecular sciences · 2021Article
- Effect of Amniotic Membrane/Collagen-Based Scaffolds on the Chondrogenic Differentiation of Adipose-Derived Stem Cells and Cartilage Repair.Frontiers in cell and developmental biology · 2021Article
- Sex Steroids and Osteoarthritis: A Mendelian Randomization Study.Frontiers in endocrinology · 2021Article
- Suppression of miR-203-3p inhibits lipopolysaccharide induced human intervertebral disc inflammation and degeneration through upregulating estrogen receptor α.Gene therapy · 2020Article
- The local and circulating SOX9 as a potential biomarker for the diagnosis of primary bone cancer.Journal of bone oncology · 2020Article
- 17β-Estradiol Induces Mitophagy Upregulation to Protect ChondrocytesFrontiers in endocrinology · 2020Article
- Does cartilage ERα overexpression correlate with osteoarthritic chondrosenescence? Indications fromJournal of biosciences · 2019Article
- Estrogen prevents articular cartilage destruction in a mouse model of AMPK deficiency via ERK-mTOR pathway.Annals of translational medicine · 2019Article
- Estrogen Promotes Mandibular Condylar Fibrocartilage Chondrogenesis and Inhibits Degeneration via Estrogen Receptor Alpha in Female Mice.Scientific reports · 2018Article
- 17β-Estradiol on the Expression of G-Protein Coupled Estrogen Receptor (GPER/GPR30) Mitophagy, and the PI3K/Akt Signaling Pathway in ATDC5 Chondrocytes In Vitro.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Protective effect of estrogen against calcification in the cartilage endplate.International journal of clinical and experimental pathology · 2018Article
- Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledThe existence of a link between estrogen deprivation and osteoarthritis (OA) in postmenopausal women suggests that 17β-estradiol (17β-E2) may be a modulator of cartilage homeostasis. Here, we demonstrate that 17β-E2 stimulates, via its receptor human estrogen receptor α 66 (hERα66), type II collagen expression in differentiated and dedifferentiated (reflecting the OA phenotype) articular chondrocytes. Transactivation of type II collagen gene (COL2A1) by ligand-independent transactivation domain (AF-1) of hERα66 was mediated by "GC" binding sites of the -266/-63-bp promoter, through physical interactions between ERα, Sp1/Sp3, Sox9, and p300, as demonstrated in chromatin immunoprecipitation (ChIP) and Re-Chromatin Immuno-Precipitation (Re-ChIP) assays in primary and dedifferentiated cells. 17β-E2 and hERα66 increased the DNA-binding activities of Sp1/Sp3 and Sox-9 to both COL2A1 promoter and enhancer regions. Besides, Sp1, Sp3, and Sox-9 small interfering RNAs (siRNAs) prevented hERα66-induced transactivation of COL2A1, suggesting that these factors and their respective cis-regions are required for hERα66-mediated COL2A1 up-regulation. Our results highlight the genomic pathway by which 17β-E2 and hERα66 modulate Sp1/Sp3 heteromer binding activity and simultaneously participate in the recruitment of the essential factors Sox-9 and p300 involved respectively in the chondrocyte-differentiated status and COL2A1 transcriptional activation. These novel findings could therefore be attractive for tissue engineering of cartilage in OA, by the fact that 17β-E2 could promote chondrocyte redifferentiation. KEY MESSAGES: 17β-E2 up-regulates type II collagen gene expression in articular chondrocytes. An ERα66/Sp1/Sp3/Sox-9/p300 protein complex mediates this stimulatory effect. This heteromeric complex interacts and binds to Col2a1 promoter and enhancer in vivo. Our findings highlight a new regulatory mechanism for 17β-E2 action in chondrocytes. 17β-E2 might be an attractive candidate for cartilage engineering applications.
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