ArticleMolecular medicine reports2018
MicroRNA‑206 contributes to the progression of steroid‑induced avascular necrosis of the femoral head by inducing osteoblast apoptosis by suppressing programmed cell death 4.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- The role of ferroptosis in osteoporosis: a cellular perspective on osteoblast, osteoclast and osteocyte dysfunction.Frontiers in endocrinology · 2026Pooled it
- Advances in the mechanism for steroid-induced osteonecrosis of the femoral head.Bone research · 2026Review
- Brain-body mechanisms contribute to sexual dimorphism in amyotrophic lateral sclerosis.Nature reviews. Neurology · 2024Review
- Knowledge mapping of programmed cell death in osteonecrosis of femoral head: a bibliometric analysis (2000-2022).Journal of orthopaedic surgery and research · 2023Review
- Article
- Interplay Between Non-Coding RNAs and Programmed Cell Death Proteins.Frontiers in oncology · 2022Review
- Administration of mircoRNA-135b-reinforced exosomes derived from MSCs ameliorates glucocorticoid-induced osteonecrosis of femoral head (ONFH) in rats.Journal of cellular and molecular medicine · 2020Article
- Extracellular vesicles from endothelial progenitor cells prevent steroid-induced osteoporosis by suppressing the ferroptotic pathway in mouse osteoblasts based on bioinformatics evidence.Scientific reports · 2019Article
- Crocin protects against dexamethasone‑induced osteoblast apoptosis by inhibiting the ROS/Ca2+‑mediated mitochondrial pathway.Molecular medicine reports · 2019Article
- Noncoding RNAs in Steroid-Induced Osteonecrosis of the Femoral Head.BioMed research international · 2019Review
- Expression of Bax/Bcl-2, TGF-β1, and Type III Collagen Fiber in Congenital Muscular Torticollis.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The expression of microRNA‑206 (miR‑206) is aberrantly induced in steroid‑induced avascular necrosis of femoral head (SANFH). Therefore, investigating the function of miR‑206 in SANFH and uncovering the functional mechanism associated with the condition will promote the understanding and treatment of the disease. The purpose of the present study was to investigate the pro‑osteoclasteogenic effect of miR‑206 that occurs through regulation of programmed cell death 4 (PDCD4). The expression of miR‑206 and PDCD4 was analyzed in the clinical SANFH specimens. The level of miR‑206 and PDCD4 was regulated in human osteoblast lineage hFOB1.19 and the effect of different treatments on cell viability, proliferation, apoptosis and differentiation potential of osteoblasts were analyzed with a Cell Counting kit‑8, 5‑ethynyl‑2'‑deoxyuridine staining, flow cytometry and Hoechst staining. The expression of miR‑206 was upregulated while PDCD4 was downregulated in the SANFH specimens. Induced expression of miR‑206 decreased cell viability and proliferation, while apoptosis was induced. At the molecular level, overexpression of miR‑206 inhibited the expression of PDCD4, alkaline phosphatase (ALP) and B‑cell lymphoma 2 (Bcl‑2), and increased the expression of apoptosis regulator Bcl2‑X‑associated protein (Bax). Inhibiting the expression of miR‑206 increased cell viability and proliferation but had no effect on cell apoptosis, as detected by flow cytometry and Hoechst staining. However, at the molecular level, inhibiting the expression of miR‑206 induced expression of PDCD4, ALP and Bcl‑2, while it decreased the expression of Bax. Additionally, knockdown of PDCD4 blocked the effect of miR‑206 inhibition on hFOB1.19 cells, representing a PDCD4‑dependent manner of miR‑206 in inducing apoptosis of osteoblasts. Therefore, miR‑206 promoted the onset of SANFH by inducing apoptosis and suppressed the proliferation of osteoblasts, which was dependent on the inhibition of PDCD4.
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