ArticleCellular & molecular biology letters2011
17β-Estradiol promotes cell proliferation in rat osteoarthritis model chondrocytes via PI3K/Akt pathway.
Article in Cellular & molecular biology letters, 2011. 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, 87 citations in OpenAlex.
- Sex hormones and their receptors in osteoarthritis: current research progress.Annals of joint · 2026Review
- HAPLN1 Exhibits Dual Effects: Facilitating Extracellular Matrix Restoration while Enhancing Inflammatory Mediator Production in Arthritic Chondrocytes.Inflammation · 2025Article
- HIF-1α regulates the proliferation and differentiation of mouse cranial base sphenoid-occipital synchondrosis chondrocytes via PI3K/Akt signaling.Scientific reports · 2025Article
- Genetic transcriptional regulation profiling of cartilage reveals pathogenesis of osteoarthritis.EBioMedicine · 2025Article
- MiR-29a-3p mediates phosphatase and tensin homolog and inhibits osteoarthritis progression.Functional & integrative genomics · 2024Article
- Calycosin ameliorates osteoarthritis by regulating the imbalance between chondrocyte synthesis and catabolism.BMC complementary medicine and therapies · 2024Article
- Bioactive components and potential mechanisms of Biqi Capsule in the treatment of osteoarthritis: based on chondroprotective and anti-inflammatory activity.Frontiers in pharmacology · 2024Article
- Low back pain and osteoarthritis pain: a perspective of estrogen.Bone research · 2023Review
- Sex-dependent variation in cartilage adaptation: from degeneration to regeneration.Biology of sex differences · 2023Review
- Morroniside inhibits Beclin1-dependent autophagic death and Bax-dependent apoptosis in cardiomyocytes through repressing BCL2 phosphorylation.In vitro cellular & developmental biology. Animal · 2023Article
- Single-cell RNA sequencing analysis of human chondrocytes reveals cell-cell communication alterations mediated by interactive signaling pathways in osteoarthritis.Frontiers in cell and developmental biology · 2023Article
- Beclin1- and Atg13-dependent autophagy activation and morroniside have synergistic effect on osteoblastogenesis.Experimental biology and medicine (Maywood, N.J.) · 2022Article
- Artemisinin relieves osteoarthritis by activating mitochondrial autophagy through reducing TNFSF11 expression and inhibiting PI3K/AKT/mTOR signaling in cartilage.Cellular & molecular biology letters · 2022Article
- The Metabolic Landscape in Osteoarthritis.Aging and disease · 2022Article
- Estrogenic impregnation alters pain expression: analysis through functional neuropeptidomics in a surgical rat model of osteoarthritis.Naunyn-Schmiedeberg's archives of pharmacology · 2022Article
- Vaspin promotes chondrogenic differentiation of BMSCs via Akt activation in osteoarthritis.BMC musculoskeletal disorders · 2022Article
- The probable role and therapeutic potential of the PI3K/AKT signaling pathway in SARS-CoV-2 induced coagulopathy.Cellular & molecular biology letters · 2022Review
- Kindlin-2 Promotes Chondrogenesis and Ameliorates IL-1beta-Induced Inflammation in Chondrocytes Cocultured with BMSCs in the Direct Contact Coculture System.Oxidative medicine and cellular longevity · 2022Article
- Osteopontin inhibits osteoarthritis progression via the OPN/CD44/PI3K signal axis.Genes & diseases · 2022Article
- The Protective Effects of Parathyroid Hormone (1-34) on Cartilage and Subchondral Bone Through Down-Regulating JAK2/STAT3 and WNT5A/ROR2 in a Collagenase-Induced Osteoarthritis Mouse Model.Orthopaedic surgery · 2021Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is the most common cause of musculoskeletal pain and disability. The importance of chondrocytes in the pathogenesis of OA is unequivocal. 17β-estradiol (E2) has a potential protective effect against OA. However, the mechanism of E2 in OA chondrocytes remains unclear. In this study, we investigated the regulative effect of E2 on cell growth and the relationship between E2 and the PI3K/Akt pathway in rat OA model chondrocytes (pretreated with interleukin-1β). We found that E2 induced chondrocyte proliferation, and increased the expression level of Akt simultaneously, especially the expression level of P-Akt. Furthermore, the inhibition of P-Akt could block chondrocyte proliferation induced by E2. These results suggest that PI3K/Akt activation induced by E2 may be an important factor in the mechanism of E2 in cell proliferation in rat OA model chondrocytes, and help further understanding the role of E2 in OA progression.
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