ArticleMedical science monitor : international medical journal of experimental and clinical research2018
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.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 57 citations in OpenAlex.
- Exercise-Induced Regulation of Bone Remodeling via Mitophagy: A Review of Current Evidence.Biomolecules · 2026Review
- Upregulation ofTranslational andrology and urology · 2026Article
- Investigating the association between uterine fibroids and weight-bearing joint osteoarthritis based on a bidirectional Mendelian randomization study.Experimental and therapeutic medicine · 2026Article
- The estrogen-ferroptosis axis in postmenopausal osteoporosis, osteoarthritis, and intervertebral disc degeneration: shared mechanisms and emerging evidence.Frontiers in immunology · 2026Review
- Serum methylmalonic acid levels predict multisite bone mineral density decline in patients with suspected mitochondrial dysfunction.Journal of orthopaedic surgery and research · 2025Article
- Fasting activates optineurin-mediated mitophagy in chondrocytes to protect against osteoarthritis.Communications biology · 2025Article
- Heat shock proteins in osteoarthritis: molecular mechanisms, pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Exosomes derived from platelet-rich plasma present a novel potential in repairing knee articular cartilage defect combined with cyclic peptide-modified β-TCP scaffold.Journal of orthopaedic surgery and research · 2024Article
- Joint Inflammation Correlates with Joint GPR30 Expression in Males and Hippocampal GPR30 Expression in Females in a Rat Model of Rheumatoid Arthritis.International journal of molecular sciences · 2024Article
- Activation of GPER1 by G1 prevents PTSD-like behaviors in mice: Illustrating the mechanisms from BDNF/TrkB to mitochondria and synaptic connection.CNS neuroscience & therapeutics · 2024Article
- Identification and Verification of Hub Mitochondrial Dysfunction Genes in Osteoarthritis Based on Bioinformatics Analysis.Journal of immunology research · 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
- GPER1 contributes to T3-induced osteogenesis by mediating glycolysis in osteoblast precursors.Experimental biology and medicine (Maywood, N.J.) · 2023Article
- MiR-196a-5p facilitates progression of estrogen-dependent endometrial cancer by regulating FOXO1.Histology and histopathology · 2023Article
- Article
- Insight into the Potential Mechanisms of Endocrine Disruption by Dietary Phytoestrogens in the Context of the Etiopathogenesis of Endometriosis.International journal of molecular sciences · 2023Review
- Sex-dependent variation in cartilage adaptation: from degeneration to regeneration.Biology of sex differences · 2023Review
- Cytochrome P450 1B1 Expression Regulates Intracellular Iron Levels and Oxidative Stress in the Retinal Endothelium.International journal of molecular sciences · 2023Article
- Expression and estrogen regulation of G protein-coupled estrogen receptor in human glioblastoma cells.Oncology letters · 2022Article
- Mitophagy-A New Target of Bone Disease.Biomolecules · 2022Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Osteoarthritis is a progressive inflammatory joint disease resulting in damage to articular cartilage. G-protein coupled estrogen receptor (GPER/GPR30) activates cell signaling in response to 17β-estradiol, which can be blocked by the GPR30 agonist, G15, an analog of G-1. The aims of this study were to investigate the effects of 17β-estradiol on the expression of G-protein coupled estrogen receptor (GPER/GPR30) on mitophagy and the PI3K/Akt signaling pathway in ATDC5 chondrocytes in vitro. MATERIAL AND METHODS Cultured ATDC5 chondrocytes were treated with increasing concentrations of 17β-estradiol with and without G15, p38 inhibitor (SB203580), JNK inhibitor (SP600125), PI3K inhibitor (LY294002, S1737), and mTOR inhibitor (S1842). Expression of GPER/GPR30 and components of the PI3K/Akt pathway in cultured ATDC5 chondrocytes were detected by immunofluorescence (IF) staining, Western blot, and real-time polymerase chain reaction (RT-PCR). Transmission electron microscopy (TEM) and IF were used to detect mitophagosomes. Expression of LC-3, LAMP2, TOM20, Hsp60, p-Akt, p-mTOR, p-p38, and p-JNK was investigated by Western blot. Proliferation and viability of the ATDC5 chondrocytes were determined using BrdU and MTT assays. RESULTS In 17β-estradiol-treated ATDC5 chondrocytes, increased expression of GPER/GPR30 was found, but fewer mitophagosomes were observed, and decreased numbers of TOM20-positive granules were co-localized with decreased LAMP2 and increased expression levels of TOM20, Hsp60, p-Akt, and p-mTOR, and reduced expression of LC3-II, were found. In 17β-estradiol-treated ATDC5 chondrocytes, the proliferation and viability of the 17β-estradiol-treated ATDC5 chondrocytes were significantly elevated. CONCLUSIONS Treatment with 17β-estradiol protected ATDC5 chondrocytes against mitophagy via the GPER/GPR30 and the PI3K/Akt signaling pathway.
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