ArticleBone2015
Defective cancellous bone structure and abnormal response to PTH in cortical bone of mice lacking Cx43 cytoplasmic C-terminus domain.
Article in Bone, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 36 citations in OpenAlex.
- Independent contribution of gonads and sex chromosomes to sex differences in bone mass and strength in the four-core genotypes mouse model.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Article
- Pannexins in the musculoskeletal system: new targets for development and disease progression.Bone research · 2024Review
- Role of Cx43 on the Bone Cell Generation, Function, and Survival.Bioelectricity · 2023Article
- Platelet-derived growth factor PDGF-AA upregulates connexin 43 expression and promotes gap junction formations in osteoblast cells throughBiochemistry and biophysics reports · 2023Article
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- Connexin 43 hemichannels and prostaglandin EFrontiers in cell and developmental biology · 2023Review
- MicroRNA-101a enhances trabecular bone accrual in male mice.Scientific reports · 2022Article
- Anabolic actions of PTH in murine models: two decades of insights.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2021Article
- Cortical bone development, maintenance and porosity: genetic alterations in humans and mice influencing chondrocytes, osteoclasts, osteoblasts and osteocytes.Cellular and molecular life sciences : CMLS · 2021Review
- Osteocytic miR21 deficiency improves bone strength independent of sex despite having sex divergent effects on osteocyte viability and bone turnover.The FEBS journal · 2020Article
- Age- and sex-dependent role of osteocytic pannexin1 on bone and muscle mass and strength.Scientific reports · 2019Article
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- Article
- Cx43 overexpression in osteocytes prevents osteocyte apoptosis and preserves cortical bone quality in aging mice.JBMR plus · 2018Article
- Connexins and Pannexins in Bone and Skeletal Muscle.Current osteoporosis reports · 2017Review
- Disruption of the Cx43/miR21 pathway leads to osteocyte apoptosis and increased osteoclastogenesis with aging.Aging cell · 2017Article
- Connexin43 and the Intercellular Signaling Network Regulating Skeletal Remodeling.Current osteoporosis reports · 2017Review
- Article
- The C-terminal domain of connexin43 modulates cartilage structure via chondrocyte phenotypic changes.Oncotarget · 2016Article
- Osteocytic signalling pathways as therapeutic targets for bone fragility.Nature reviews. Endocrinology · 2016Review
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
Connexin 43 (Cx43) forms gap junction channels and hemichannels that allow the communication among osteocytes, osteoblasts, and osteoclasts. Cx43 carboxy-terminal (CT) domain regulates channel opening and intracellular signaling by acting as a scaffold for structural and signaling proteins. To determine the role of Cx43 CT domain in bone, mice in which one allele of full length Cx43 was replaced by a mutant lacking the CT domain (Cx43(ΔCT/fl)) were studied. Cx43(ΔCT/fl) mice exhibit lower cancellous bone volume but higher cortical thickness than Cx43(fl/fl) controls, indicating that the CT domain is involved in normal cancellous bone gain but opposes cortical bone acquisition. Further, Cx43(ΔCT) is able to exert the functions of full length osteocytic Cx43 on cortical bone geometry and mechanical properties, demonstrating that domains other than the CT are responsible for Cx43 function in cortical bone. In addition, parathyroid hormone (PTH) failed to increase endocortical bone formation or energy to failure, a mechanical property that indicates resistance to fracture, in cortical bone in Cx43(ΔCT) mice with or without osteocytic full length Cx43. On the other hand, bone mass and bone formation markers were increased by the hormone in all mouse models, regardless of whether full length or Cx43(ΔCT) were or not expressed. We conclude that Cx43 CT domain is involved in proper bone acquisition; and that Cx43 expression in osteocytes is dispensable for some but not all PTH anabolic actions.
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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.