ArticlePloS one2011
Overexpression of Bcl2 in osteoblasts inhibits osteoblast differentiation and induces osteocyte apoptosis.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 67 citations in OpenAlex.
- Regulated cell death in musculoskeletal development, homeostasis, and diseases.Fundamental research · 2026Review
- Engineering Efferocytosis for Bone Regeneration.Macromolecular bioscience · 2025Review
- Osteogenic Potential of Simvastatin and Fluvastatin in an Organotypic Bone Model.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Screening, Analysis, and Validation of Endoplasmic Reticulum Stress-Related DEGs in Epilepsy.Cellular and molecular neurobiology · 2025Article
- Bcl-2 and Bcl-xL in Diabetes: Contributions to Endocrine Pancreas Viability and Function.Biomedicines · 2025Review
- The Roles of Forkhead Box O3a (FOXO3a) in Bone and Cartilage Diseases - A Narrative Review.Drug design, development and therapy · 2025Review
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- Efferocytosis and Bone Dynamics.Current osteoporosis reports · 2024Review
- Induction of osteoblast apoptosis stimulates macrophage efferocytosis and paradoxical bone formation.Bone research · 2024Article
- Emerging Roles of Natural Compounds in Osteoporosis: Regulation, Molecular Mechanisms and Bone Regeneration.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Roles of Sp7 in osteoblasts for the proliferation, differentiation, and osteocyte process formation.Journal of orthopaedic translation · 2024Article
- Identification of miRNAs related to osteoporosis by high-throughput sequencing.Frontiers in pharmacology · 2024Article
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- miR-126 mitigates the osteogenic differentiation of human bone marrow-derived mesenchymal stem cells by targeting the ERK1/2 and Bcl-2 pathways.Acta biochimica et biophysica Sinica · 2023Article
- Transcriptome-wide association study identifies novel genes associated with bone mineral density and lean body mass in children.Endocrine · 2023Article
- Article
- Molecular mechanism of a novel root-end filling material containing zirconium oxide on the osteogenic/odontogenic differentiation of human osteosarcoma MG-63 cells.Frontiers in bioengineering and biotechnology · 2023Article
- Osteocytes: Their Lacunocanalicular Structure and Mechanoresponses.International journal of molecular sciences · 2022Review
- Sp7 Transgenic Mice with a Markedly Impaired Lacunocanalicular Network Induced Sost and Reduced Bone Mass by Unloading.International journal of molecular sciences · 2022Article
- Uncovering Hidden Mechanisms of Different Prescriptions Treatment for OsteoporosisFrontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bcl2 subfamily proteins, including Bcl2 and Bcl-X(L), inhibit apoptosis. As osteoblast apoptosis is in part responsible for osteoporosis in sex steroid deficiency, glucocorticoid excess, and aging, bone loss might be inhibited by the upregulation of Bcl2; however, the effects of Bcl2 overexpression on osteoblast differentiation and bone development and maintenance have not been fully investigated. To investigate these issues, we established two lines of osteoblast-specific BCL2 transgenic mice. In BCL2 transgenic mice, bone volume was increased at 6 weeks of age but not at 10 weeks of age compared with wild-type mice. The numbers of osteoblasts and osteocytes increased, but osteoid thickness and the bone formation rate were reduced in BCL2 transgenic mice with high expression at 10 weeks of age. The number of BrdU-positive cells was increased but that of TUNEL-positive cells was unaltered at 2 and 6 weeks of age. Osteoblast differentiation was inhibited, as shown by reduced Col1a1 and osteocalcin expression. Osteoblast differentiation of calvarial cells from BCL2 transgenic mice also fell in vitro. Overexpression of BCL2 in primary osteoblasts had no effect on osteoclastogenesis in co-culture with bone marrow cells. Unexpectedly, overexpression of BCL2 in osteoblasts eventually caused osteocyte apoptosis. Osteocytes, which had a reduced number of processes, gradually died with apoptotic structural alterations and the expression of apoptosis-related molecules, and dead osteocytes accumulated in cortical bone. These findings indicate that overexpression of BCL2 in osteoblasts inhibits osteoblast differentiation, reduces osteocyte processes, and causes osteocyte apoptosis.
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