ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2008
Vitamin D receptor-dependent 1 alpha,25(OH)2 vitamin D3-induced anti-apoptotic PI3K/AKT signaling in osteoblasts.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
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Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- The role of vitamin D signalling in β cell apoptosis: a systematic review.Apoptosis : an international journal on programmed cell death · 2026Pooled it
- Vitamin DThe American journal of clinical nutrition · 2025Trial
- Vitamin DJournal of cachexia, sarcopenia and muscle · 2021Trial
- Increased telomerase activity and vitamin D supplementation in overweight African Americans.International journal of obesity (2005) · 2012Trial
- Vitamin D decreases tumor cell growth and invasiveness in primary malignant bone tumors in vitro.Journal of bone oncology · 2026Article
- The role and therapeutic potential of vitamins in fracture healing.Nutrition journal · 2026Review
- Vitamin D receptor signaling in inflammatory senescence-associated skin aging: Mechanisms and therapeutic potentials.Journal of cell communication and signaling · 2026Article
- The TLR10-Vitamin D Axis Facilitates Osteogenic Differentiation of Mesenchymal Stem Cells In Vitro.Cells · 2026Article
- Decoding the secretory blueprint of bone healing: from gradients to regeneration.Frontiers in cell and developmental biology · 2026Review
- Review
- Vitamin D3 Exerts Beneficial Effects on C2C12 Myotubes through Activation of the Vitamin D Receptor (VDR)/Sirtuins (SIRT)1/3 Axis.Nutrients · 2023Article
- 1,25(OH)Oxidative medicine and cellular longevity · 2022Article
- Role of vitamin D in diabetic retinopathy: Pathophysiological and clinical aspects.Reviews in endocrine & metabolic disorders · 2021Review
- 1ɑ,25-Dihydroxyvitamin DJournal of cellular and molecular medicine · 2021Article
- Vitamin K and D Supplementation and Bone Health in Chronic Kidney Disease-Apart or Together?Nutrients · 2021Review
- A Newly Identified lncBCAS1-4_1 Associated With Vitamin D Signaling and EMT in Ovarian Cancer Cells.Frontiers in oncology · 2021Article
- Article
- Vitamin D receptor (VDR) and metabolizing enzymes CYP27B1 and CYP24A1 in breast cancer.Molecular biology reports · 2020Review
- Vitamin D actions in neurons require the PI3K pathway for both enhancing insulin signaling and rapid depolarizing effects.The Journal of steroid biochemistry and molecular biology · 2020Article
- RNAi-mediated knockdown of VDR surprisingly suppresses cell growth in Jurkat T and U87-MG cells.Heliyon · 2019Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Osteoblast apoptosis plays a crucial role in bone remodeling. Physiological doses of 1 alpha,25(OH)(2)-vitamin D(3) (1,25D) protect osteoblasts against apoptosis by means of mechanisms only partially understood. We studied activation of an Akt survival cascade downstream of 1,25D nongenomic stimulation of phosphatidylinositide-3'-kinase (PI3K) in osteoblastic cells. We measured a dose- and time-dependent 1,25D induction of Akt phosphorylation (p-Akt) in cultured osteoblastic cells. Maximal response was achieved with 10 nM 1,25D after 5 min. We found that staurosporine (STSP)-induced apoptosis was significantly reduced in 1,25D-pretreated osteoblasts. 1,25D prosurvival effects were abolished when cells were preincubated with inhibitors of PI3K activation. By means of siRNA silencing, we proved that 1,25D induction of p-Akt requires a classic vitamin D receptor (VDR) in osteoblasts. Furthermore, non-osteoblastic CV-1 cells transfected with an enhanced green fluorescent protein (EGFP)-VDR construct responded to 1,25D treatment with a rapid p-Akt response associated with increased cell survival not detected in native, nontransfected cells. We measured increased levels of p-Akt substrates p-Bad and p-FKHR and significantly reduced activity of caspases 8 and 3/7 after 1,25D treatment. In addition, 1,25D-induced protection against apoptosis was abolished when osteoblasts were preincubated with pertussis toxin. We conclude that anti-apoptotic effects of 1,25D in osteoblasts occur through nongenomic activation of a VDR/PI3K/Akt survival pathway that includes phosphorylation of multiple p-Akt substrates and reduction of caspase activities.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.