ArticleJournal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research2009
Ethanol impairs estrogen receptor signaling resulting in accelerated activation of senescence pathways, whereas estradiol attenuates the effects of ethanol in osteoblasts.
Article in Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 78 citations in OpenAlex.
- Article
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- Estradiol Modulates the Sensitivity to Vancomycin ofMicroorganisms · 2025Article
- Quantification of Pesticides and In Vitro Effects of Water-Soluble Fractions of Agricultural Soils in South Africa.Archives of environmental contamination and toxicology · 2025Article
- In vitro endocrine and cardiometabolic toxicity associated with artificial turf materials.Environmental toxicology and pharmacology · 2024Article
- The impact of ageing mechanisms on musculoskeletal system diseases in the elderly.Frontiers in immunology · 2024Review
- Biological Effects of "Inflammageing" on Human Oral Cells: Insights into a Potential Confounder of Age-Related Diseases.International journal of molecular sciences · 2023Article
- Colchicine Protects against Ethanol-Induced Senescence and Senescence-Associated Secretory Phenotype in Endothelial Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Targeting cellular senescence in senile osteoporosis: therapeutic potential of traditional Chinese medicine.Frontiers in medicine · 2023Review
- Senescent cells: A therapeutic target for osteoporosis.Cell proliferation · 2022Review
- Nox4 expression in osteo-progenitors controls bone development in mice during early life.Communications biology · 2022Article
- Episodic alcohol exposure attenuates mesenchymal stem cell chondrogenic differentiation during bone fracture callus formation.Alcoholism, clinical and experimental research · 2022Article
- Estrogen prevents cellular senescence and bone loss through Usp10-dependent p53 degradation in osteocytes and osteoblasts: the role of estrogen in bone cell senescence.Cell and tissue research · 2021Article
- Effects of graded increases in ethanol consumption on biochemical markers of bone turnover in young adult male cynomolgus macaques.Alcohol (Fayetteville, N.Y.) · 2021Article
- Impact of Alcohol on Bone Health, Homeostasis and Fracture repair.Current pathobiology reports · 2020Article
- Nox4 Expression Is Not Required for OVX-Induced Osteoblast Senescence and Bone Loss in Mice.JBMR plus · 2020Article
- Effects of Chronic Ethanol Consumption and Ovariectomy on the Spontaneous Alveolar Bone Loss in Rats.International journal of dentistry · 2020Article
- Voluntary Chronic Heavy Alcohol Consumption in Male Rhesus Macaques Suppresses Cancellous Bone Formation and Increases Bone Marrow Adiposity.Alcoholism, clinical and experimental research · 2019Article
- Effects of Alcohol and Estrogen Receptor Blockade Using ICI 182,780 on Bone in Ovariectomized Rats.Alcoholism, clinical and experimental research · 2019Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Epidemiological and animal studies have suggested that chronic alcohol consumption is a major risk factor for osteoporosis. Using bone from cycling female rats infused chronically with ethanol (EtOH) in vivo and osteoblastic cells in vitro, we found that EtOH significantly increased estrogen receptor alpha (ERalpha) and beta (ERbeta) mRNA and ERalpha protein levels. Treatment with 17beta-estradiol (E2) in vivo and in vitro interfered with these effects of EtOH on bone and osteoblastic cells. ERalpha agonist propylpyrazoletriol (PPT) and ERbeta agonist diarylpropionitrile (DPN) attenuated EtOH-induced ERalpha and ERbeta gene overexpression, respectively. Similar to the ER antagonist ICI 182780, EtOH blocked nuclear translocation of ERalpha-ECFP in the presence of E2 in UMR-106 osteoblastic cells. EtOH also downregulated ERE-luc reporter activity. On the other hand, EtOH by itself upregulated some common ERalpha- and ERbeta-mediated genes apparently by an ER-independent pathway. EtOH also transactivated the luciferase activity of the p21 promoter region independent of additional exogenous ERalpha, activated p21 and p53, and stimulated senescence-associated beta-galactosidase activity in rat stromal osteoblasts. E2 treatment attenuated these EtOH actions. We conclude that inhibitory cross-talk between EtOH and E2 in osteoblasts on ERs, p53/p21, and cell senescence provides a pathophysiologic mechanism underlying bone loss and the protective effects of estrogens in alcohol-exposed females.
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