ArticleJournal of orthopaedic research : official publication of the Orthopaedic Research Society2012
Age-related changes in gap junctional intercellular communication in osteoblastic cells.
Article in Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 37 citations in OpenAlex.
- Green Tea Mitigates the Hallmarks of Aging and Age-Related Multisystem Deterioration.Aging and disease · 2025Review
- Impact of Environmental and Epigenetic Changes on Mesenchymal Stem Cells during Aging.International journal of molecular sciences · 2023Review
- Aging Hallmarks and the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- ATP transporters in the joints.Purinergic signalling · 2021Review
- A bioelectric model of carcinogenesis, including propagation of cell membrane depolarization and reversal therapies.Scientific reports · 2021Article
- Bisphenol S enhances gap junction intercellular communication in ovarian theca cells.Chemosphere · 2021Article
- Bone marrow mesenchymal stem cells: Aging and tissue engineering applications to enhance bone healing.Biomaterials · 2019Review
- Transforming growth factor-β1 up-regulates connexin43 expression in osteocytes via canonical Smad-dependent signaling pathway.Bioscience reports · 2018Article
- Gap junctional communication is involved in differentiation of osteoclasts from bone marrow and peripheral blood monocytes.Heliyon · 2018Article
- Joint diseases: from connexins to gap junctions.Nature reviews. Rheumatology · 2017Review
- 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
- Role of connexins and pannexins during ontogeny, regeneration, and pathologies of bone.BMC cell biology · 2016Review
- Connexins and pannexins in the skeleton: gap junctions, hemichannels and more.Cellular and molecular life sciences : CMLS · 2015Review
- American Society of Biomechanics Journal of Biomechanics Award 2013: cortical bone tissue mechanical quality and biological mechanisms possibly underlying atypical fractures.Journal of biomechanics · 2015Review
- Sclerostin is expressed in osteoclasts from aged mice and reduces osteoclast-mediated stimulation of mineralization.Journal of cellular biochemistry · 2013Article
- Connexin 43 channels protect osteocytes against oxidative stress-induced cell death.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2013Article
- Functional impairment of bone formation in the pathogenesis of osteoporosis: the bone marrow regenerative competence.Current osteoporosis reports · 2013Review
- Impaired function of the blood-testis barrier during aging is preceded by a decline in cell adhesion proteins and GTPases.PloS one · 2013Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Aging demonstrates deleterious effects upon the skeleton which can predispose an individual to osteoporosis and related fractures. Despite the well-documented evidence that aging decreases bone formation, there remains little understanding whereby cellular aging alters skeletal homeostasis. We, and others, have previously demonstrated that gap junctions--membrane-spanning channels that allow direct cell-to-cell conductance of small signaling molecules--are critically involved in osteoblast differentiation and skeletal homeostasis. We examined whether the capacity of rat osteoblastic cells to form gap junctions and respond to known modulators of gap junction intercellular communication (GJIC) was dependent on the age of the animal from which they were isolated. We observed no effect of age upon osteoblastic Cx43 mRNA, protein or GJIC. We also examined age-related changes in PTH-stimulated GJIC. PTH demonstrated age-dependent effects upon GJIC: Osteoblastic cells from young rats increased GJIC in response to PTH, whereas there was no change in GJIC in response to PTH in osteoblastic cells from mature or old rats. PTH-stimulated GJIC occurred independently of changes in Cx43 mRNA or protein expression. Cholera toxin significantly increased GJIC in osteoblastic cells from young rats compared to those from mature and old rats. These data demonstrate an age-related impairment in the capacity of osteoblastic cells to generate functional gap junctions in response to PTH, and suggest that an age-related defect in G protein-coupled adenylate cyclase activity at least partially contributes to decreased PTH-stimulated GJIC.
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.