ArticleMolecular medicine reports2020
1,25(OH)2D3 inhibits osteogenic differentiation through activating β‑catenin signaling via downregulating bone morphogenetic protein 2.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Vitamin D and the aging skin: insights into oxidative stress, inflammation, and barrier function.Immunity & ageing : I & A · 2025Review
- Imbalance of early-life vitamin D intake targets ROS-mediated crosstalk between mitochondrial dysfunction and differentiation potential of MSCs associated the later obesity.Stem cell research & therapy · 2024Article
- Article
- Epigenetic regulation of mesenchymal stem cell aging through histone modifications.Genes & diseases · 2023Review
- 1,25(OH)Experimental and therapeutic medicine · 2023Article
- Vitamin D Alleviates Cadmium-Induced Inhibition of Chicken Bone Marrow Stromal Cells' Osteogenic Differentiation In Vitro.Animals : an open access journal from MDPI · 2023Article
- The Relationship between Renin-Angiotensin-Aldosterone System (RAAS) Activity, Osteoporosis and Estrogen Deficiency in Type 2 Diabetes.International journal of molecular sciences · 2023Review
- Effects of vitamin D with or without calcium on pathological ossification: A retrospective clinical study.Experimental and therapeutic medicine · 2022Article
- Pharmacological Manipulation of Wnt/β-Catenin Signaling Pathway in Human Neural Precursor Cells Alters Their Differentiation Potential and Neuronal Yield.Frontiers in molecular neuroscience · 2021Article
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The present study explored whether bone morphogenetic proteins (BMPs) and Wnt/β‑catenin signaling pathways were involved in the 1,25(OH)2D3‑induced inhibition of osteogenic differentiation in bone marrow‑derived mesenchymal stem cells (BMSCs). To evaluate the osteogenic differentiation of BMSCs, the expression levels of ossification markers, including BMP2, Runt‑related transcription factor 2 (Runx2), Msh homeobox 2 (Msx2), osteopontin (OPN) and osteocalcin (OCN), and the activity of alkaline phosphatase (ALP), as well as the calcified area observed by Alizarin red‑S staining, were investigated. Chromatin immunoprecipitation (ChIP) assay was used to detect the effect of 1,25(OH)2D3 on the DNA methylation and histone modification of BMP2, while an immunoprecipitation (IP) assay was performed to assess the crosstalk between Smad1 and disheveled‑1 (Dvl‑1) proteins. It was observed that 1,25(OH)2D3 significantly decreased the expression levels of BMP2, Runx2, Msx2, OPN and OCN, and reduced ALP activity and the calcified area in BMSCs, whereas these effects were rescued by BMP2 overexpression. ChIP assay revealed that BMSCs treated with 1,25(OH)2D3 exhibited a significant increase in H3K9me2 level and a decrease in the acetylation of histone H3 at the same BMP2 promoter region. In addition, 1,25(OH)2D3 treatment promoted the nuclear accumulation of β‑catenin by downregulating BMP2. Furthermore, the β‑catenin signaling inhibitor XAV‑939 weakened the inhibitory effect of 1,25(OH)2D3 on osteogenic differentiation. Additionally, knockdown of β‑catenin rescued the attenuation in Dvl‑1 and Smad1 interaction caused by 1,25(OH)2D3. Overexpression of Smad1 also reversed the inhibitory effect of 1,25(OH)2D3 on osteogenic differentiation. Taken together, the current study demonstrated that 1,25(OH)2D3 inhibited the differentiation of BMSCs into osteoblast‑like cells by inactivating BMP2 and activating Wnt/β‑catenin signaling.
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