ArticleLaboratory investigation; a journal of technical methods and pathology2010
Fas receptor is required for estrogen deficiency-induced bone loss in mice.
Article in Laboratory investigation; a journal of technical methods and pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- ECSIT is essential for RANKL-induced stimulation of mitochondria in osteoclasts and a target for the anti-osteoclastogenic effects of estrogens.Frontiers in endocrinology · 2023Article
- Does Aging Activate T-cells to Reduce Bone Mass and Quality?Current osteoporosis reports · 2022Review
- Bone resorption improvement by conditioned medium of stem cells from human exfoliated deciduous teeth in ovariectomized mice.Experimental and therapeutic medicine · 2022Article
- Recent Advances in Osteoclast Biological Behavior.Frontiers in cell and developmental biology · 2021Review
- Sexual Dimorphism in Osteoclasts.Cells · 2020Review
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors.Scientific reports · 2020Article
- Ovariectomy Activates Chronic Low-Grade Inflammation Mediated by Memory T Cells, Which Promotes Osteoporosis in Mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Positive and negative regulators of osteoclast apoptosis.Bone reports · 2019Review
- The Potential of Probiotics as a Therapy for Osteoporosis.Microbiology spectrum · 2017Review
- Increased chemotaxis and activity of circulatory myeloid progenitor cells may contribute to enhanced osteoclastogenesis and bone loss in the C57BL/6 mouse model of collagen-induced arthritis.Clinical and experimental immunology · 2016Article
- Modulation of unloading-induced bone loss in mice with altered ERK signaling.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Article
- Osteoblast-induced osteoclast apoptosis by fas ligand/FAS pathway is required for maintenance of bone mass.Cell death and differentiation · 2015Article
- Technetium-99 conjugated with methylene diphosphonate ameliorates ovariectomy-induced osteoporotic phenotype without causing osteonecrosis in the jaw.Calcified tissue international · 2012Article
- Chemotactic and immunoregulatory properties of bone cells are modulated by endotoxin-stimulated lymphocytes.Inflammation · 2012Article
- A new regulator of osteoclastogenesis: estrogen response element-binding protein in bone.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2011Article
- Targeting Fas in osteoresorptive disorders.Expert opinion on therapeutic targets · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Bone mass is determined by bone cell differentiation, activity, and death, which mainly occur through apoptosis. Apoptosis can be triggered by death receptor Fas (CD95), expressed on osteoblasts and osteoclasts and may be regulated by estrogen. We have previously shown that signaling through Fas inhibits osteoblast differentiation. In this study we analyzed Fas as a possible mediator of bone loss induced by estrogen withdrawal. At 4 weeks after ovariectomy (OVX), Fas gene expression was greater in osteoblasts and lower in osteoclasts in ovariectomized C57BL/6J (wild type (wt)) mice compared with sham-operated animals. OVX was unable to induce bone loss in mice with a gene knockout for Fas (Fas -/- mice). The number of osteoclasts increased in wt mice after OVX, whereas it remained unchanged in Fas -/- mice. OVX induced greater stimulation of osteoblastogenesis in Fas -/- than in wt mice, with higher expression of osteoblast-specific genes. Direct effects on bone cell differentiation and apoptosis in vivo were confirmed in vitro, in which addition of estradiol decreased Fas expression and partially abrogated the apoptotic and differentiation-inhibitory effect of Fas in osteoblast lineage cells, while having no effect on Fas-induced apoptosis in osteoclast lineage cells. In conclusion, the Fas receptor has an important role in the pathogenesis of postmenopausal osteoporosis by mediating apoptosis and inhibiting differentiation of osteoblast lineage cells. Modulation of Fas effects on bone cells may be used as a therapeutic target in the treatment of osteoresorptive disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.