ArticleThe Journal of biological chemistry2009
Transforming growth factor-beta1 (TGF-beta1) induces human osteoclast apoptosis by up-regulating Bim.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 83 citations in OpenAlex.
- Trial
- The Role of Oral and Gut Microbiota in Bone Health: Insights from Bacterial Extracellular Vesicles.Microorganisms · 2025Review
- Serum IL-6 and TGF-β1 concentrations as diagnostic biomarkers in elderly male patients with osteoporosis.European spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society · 2025Article
- The balance between helper T 17 and regulatory T cells in osteoimmunology and relevant research progress on bone tissue engineering.Immunity, inflammation and disease · 2024Review
- Review
- The roles and regulatory mechanisms of TGF-β and BMP signaling in bone and cartilage development, homeostasis and disease.Cell research · 2024Review
- Extracellular Signal-Regulated Kinases Play Essential but Contrasting Roles in Osteoclast Differentiation.International journal of molecular sciences · 2023Review
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Review
- Modeling osteoporosis to design and optimize pharmacological therapies comprising multiple drug types.eLife · 2022Article
- Bone remodeling: an operational process ensuring survival and bone mechanical competence.Bone research · 2022Review
- TGFβ reprograms TNF stimulation of macrophages towards a non-canonical pathway driving inflammatory osteoclastogenesis.Nature communications · 2022Article
- Integrated computational and in vivo models reveal Key Insights into macrophage behavior during bone healing.PLoS computational biology · 2022Article
- The Rising Era of "Immunoporosis": Role of Immune System in the Pathophysiology of Osteoporosis.Journal of inflammation research · 2022Review
- New Insights Into Osteoclast Biology.JBMR plus · 2021Review
- Role of rhBMP-7, Fibronectin, And Type I Collagen in Dental Implant Osseointegration Process: An Initial Pilot Study on Minipig Animals.Materials (Basel, Switzerland) · 2021Article
- Aberrant Bone Homeostasis in AML Is Associated with Activated Oncogenic FLT3-Dependent Cytokine Networks.Cells · 2020Article
- Influence of the TGF-β Superfamily on Osteoclasts/Osteoblasts Balance in Physiological and Pathological Bone Conditions.International journal of molecular sciences · 2020Review
- Positive and negative regulators of osteoclast apoptosis.Bone reports · 2019Review
- The Effects of TGF-β Signaling on Cancer Cells and Cancer Stem Cells in the Bone Microenvironment.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transforming growth factor-beta1 (TGF-beta1) is the most abundant TGF-beta isoform detected in bone and is an important functional modulator of osteoclasts. TGF-beta1 can induce osteoclast apoptosis; however, the apoptotic pathways involved in this process are not known. We show here that human osteoclasts express both type-I and type-II TGF-beta receptors. In the absence of survival factors, TGF-beta1 (1 ng/ml) induced osteoclast apoptosis. The expression of activated caspase-9, but not that of caspase-8, was increased by TGF-beta1 stimulation, and the rate of TGF-beta1-induced apoptosis was significantly lower in the presence of a caspase-9 inhibitor. To study further the mechanisms involved in TGF-beta1-induced osteoclast apoptosis, we investigated TGF-beta1 signaling, which primarily involves the Smad pathway, but also other pathways that may interfere with intracellular modulators of apoptosis, such as mitogen-activated protein (MAP) kinases and Bcl2 family members. We show here that early events consisted of a trend toward increased expression of extracellular signal-regulated kinase (ERK), and then TGF-beta1 significantly induced the activation of p38 and Smad2 in a time-dependent manner. These signaling cascades may activate the intrinsic apoptosis pathway, which involves Bim, the expression of which was increased in the presence of TGF-beta1. Furthermore, the rate of TGF-beta1-induced osteoclast apoptosis was lower when Bim expression was suppressed, and inhibiting the Smad pathway abolished Bim up-regulation following TGF-beta stimulation. This could correspond to a regulatory mechanism involved in the inhibition of osteoclast activity by TGF-beta1.
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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.