ArticleAlcoholism, clinical and experimental research2008
Identification of novel bone-specific molecular targets of binge alcohol and ibandronate by transcriptome analysis.
Article in Alcoholism, clinical and experimental research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Linking metabolic syndrome with low bone mass through insights from BMI and health behaviors.Scientific reports · 2023Article
- Bone Marrow Multipotent Mesenchymal Stromal Cells as Autologous Therapy for Osteonecrosis: Effects of Age and Underlying Causes.Bioengineering (Basel, Switzerland) · 2021Review
- Alcohol-induced Wnt signaling inhibition during bone fracture healing is normalized by intermittent parathyroid hormone treatment.Animal models and experimental medicine · 2020Article
- Postnatal Ethanol-Induced Neurodegeneration Involves CB1R-Mediated β-Catenin Degradation in Neonatal Mice.Brain sciences · 2020Article
- Cellular and molecular mechanisms of alcohol-induced osteopenia.Cellular and molecular life sciences : CMLS · 2017Review
- Alcohol Regulates BK Surface Expression via Wnt/β-Catenin Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- Alcohol: A Simple Nutrient with Complex Actions on Bone in the Adult Skeleton.Alcoholism, clinical and experimental research · 2016Review
- Alcohol consumption induces global gene expression changes in VTA dopaminergic neurons.Genes, brain, and behavior · 2016Article
- Identification of gene expression profile in the rat brain resulting from acute alcohol intoxication.Molecular biology reports · 2014Article
- CaMKII represses transcriptionally active β-catenin to mediate acute ethanol neurodegeneration and can phosphorylate β-catenin.Journal of neurochemistry · 2014Article
- Acute alcohol exposure impairs fracture healing and deregulates β-catenin signaling in the fracture callus.Alcoholism, clinical and experimental research · 2012Article
- Antioxidant therapy attenuates deficient bone fracture repair associated with binge alcohol exposure.Journal of orthopaedic trauma · 2011Article
- Calcium-mediated repression of β-catenin and its transcriptional signaling mediates neural crest cell death in an avian model of fetal alcohol syndrome.Birth defects research. Part A, Clinical and molecular teratology · 2011Article
- Effects of nutrition and alcohol consumption on bone loss.Current osteoporosis reports · 2011Review
- Alcohol exposure and mechanisms of tissue injury and repair.Alcoholism, clinical and experimental research · 2011Review
- Inhibition of NADPH oxidases prevents chronic ethanol-induced bone loss in female rats.The Journal of pharmacology and experimental therapeutics · 2011Article
- A role for ethanol-induced oxidative stress in controlling lineage commitment of mesenchymal stromal cells through inhibition of Wnt/beta-catenin signaling.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2010Article
- Genome-wide association study of alcohol dependence implicates a region on chromosome 11.Alcoholism, clinical and experimental research · 2010Article
- Binge alcohol-induced bone damage is accompanied by differential expression of bone remodeling-related genes in rat vertebral bone.Calcified tissue international · 2009Article
- Long-term modulations in the vertebral transcriptome of adolescent-stage rats exposed to binge alcohol.Alcohol and alcoholism (Oxford, Oxfordshire)Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundOur laboratory established that binge alcohol-related bone damage is prevented by aminobisphosphonates, suggesting bone resorption increases following binge exposure. We examined the effects of binge alcohol and antiresorptive therapy on the relationship between bone damage and modulation of the vertebral transcriptome, in an attempt to determine how alcohol-induced bone damage and its prevention modulate bone-related biological pathways.
methodsMale Sprague-Dawley rats were assigned to 1 of 6 treatment groups (n = 12/group). (C1) saline ip 3 d/wk for 1 week, (A1) binge alcohol, 3 g/kg, ip 3 d/wk for 1 week, (C4) saline ip, 3 d/wk for 4 weeks, (A4) binge alcohol, ip, 3 g/kg 3 d/wk for 4 weeks, (I4) ibandronate, saline ip 3 d/wk for 4 weeks, plus a single ip injection of ibandronate at 120 microg/animal, and (AI4) binge alcohol plus ibandronate as above. After 1 or 4 weeks, adjacent lumbar vertebrae were assayed for bone damage or transcriptional changes.
resultsBone loss was not observed after 1 week of binge alcohol treatment. After 4 weeks, binge alcohol decreased vertebral BMD by 23% (p < 0.05) and compressive strength by 18% compared to saline controls (p < 0.05). Concurrent ibandronate prevented bone loss, increasing these parameters by 145 and 134% respectively compared to binge alcohol. (p < 0.05). Analysis of the vertebral transcriptome identified gene clusters specific for acute and chronic binge alcohol-related bone damage. Acute binge alcohol modulated the expression of integrin signaling-specific genes, while chronic binge alcohol modulated canonical Wnt signaling gene expression. Ibandronate normalized the expression of approximately 20% of the genes affected by chronic binge alcohol, allowing the identification of a unique subset of alcohol-sensitive, ibandronate-responsive genes.
conclusionsIdentification of bone-specific gene expression clusters associated with acute and chronic binge alcohol treatment allowed for the identification of cellular pathways affected by binge treatment with known involvement in bone remodeling (Integrin, Canonical Wnt signaling) not previously identified as alcohol-sensitive. This data provides a basis for a plausible mechanistic explanation for the known detrimental effects of alcohol on bone formation and resorption.
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