Protective Effects of Estradiol on Ethanol-Induced Bone Loss Involve Inhibition of Reactive Oxygen Species Generation in Osteoblasts and Downstream Activation of the Extracellular Signal-Regulated Kinase/Signal Transducer and Activator of Transcription 3/Receptor Activator of Nuclear Factor-κB Ligan

@article{Chen2008ProtectiveEO,
  title={Protective Effects of Estradiol on Ethanol-Induced Bone Loss Involve Inhibition of Reactive Oxygen Species Generation in Osteoblasts and Downstream Activation of the Extracellular Signal-Regulated Kinase/Signal Transducer and Activator of Transcription 3/Receptor Activator of Nuclear Factor-$\kappa$B Ligan},
  author={Jin-Ran Chen and Kartik Shankar and Shanmugam Nagarajan and T M Badger and Martin J Ronis},
  journal={Journal of Pharmacology and Experimental Therapeutics},
  year={2008},
  volume={324},
  pages={50 - 59}
}
Bone loss occurs following chronic ethanol (EtOH) consumption in males and cycling females in part as a result of increased bone resorption. We have demonstrated in vivo that estradiol treatment can reverse this effect. Using osteoclast precursors from bone marrow and osteoblast/preosteoclast coculture, we found that EtOH-induced receptor activator of nuclear factor-κB ligand (RANKL) expression in osteoblasts was able to promote osteoclastogenesis. These effects were blocked by pretreatment of… 
Inhibition of NADPH Oxidases Prevents Chronic Ethanol-Induced Bone Loss in Female Rats
TLDR
In a rat model in which cycling females were infused intragastrically with EtOH-containing liquid diets, EtOH significantly decreased bone formation and stimulated osteoblast-dependent osteoclast differentiation, and these effects were reversed by exogenous 17-β-estradiol coadministration.
Loss of functional NADPH oxidase 2 protects against alcohol-induced bone resorption in female p47phox-/- mice.
TLDR
In osteoblasts, NOX2 and NOX4 appear to work in tandem to increase RANKL expression, whereas EtOH-mediated inhibition of bone formation occurs via a NoX2-independent mechanism, which suggests that NOx2-derived ROS is necessary for Etoh-induced bone resorption.
Role of reactive oxygen species in angiotensin II: induced receptor activator of nuclear factor-κB ligand expression in mouse osteoblastic cells
TLDR
Results suggest that Ang II, through its AT1R, enhanced NOX activity and ROS production, and activated the ERK pathway to up-regulate RANKL expression in osteoblasts in vitro.
A Role for Ethanol-Induced Oxidative Stress in Controlling Lineage Commitment of Mesenchymal Stromal Cells Through Inhibition of Wnt/β-Catenin Signaling
TLDR
Real‐time array analysis of total RNA isolated from bone tissue revealed that the majority of Wnt signaling components were downregulated by chronic ethanol infusion, consistent with the hypothesis that ethanol inhibits bone formation through stimulation of oxidative stress to suppress Wnt signalling.
Ormeloxifene inhibits osteoclast differentiation in parallel to downregulating RANKL-induced ROS generation and suppressing the activation of ERK and JNK in murine RAW264.7 cells.
TLDR
It is demonstrated that Orm potentially inhibits osteoclastogenesis by inhibiting ROS generation and thereby suppressing the activation of ERK1/2 (MAPK3/MAPK1) and JNK ( MAPK8) and transcription factors (NF-κB and AP-1), which subsequently affect the regulation of osteOClastogenesis.
Ormeloxifene inhibits osteocla st differentiation in parallel to downregulating RANKL-induced ROS generation and suppressing the activation of ERK and JNK in murine RAW 264 . 7 cells
Ormeloxifene (Orm), a triphenylethylene compound, has been established as a selective estrogen receptor modulator (SERM) that suppresses the ovariectomy-induced bone resorption in rats. However, the
Disulfiram suppressed ethanol promoted RANKL-induced osteoclastogenesis in vitro and ethanol-induced osteoporosis in vivo via ALDH1A1-NFATc1 axis
TLDR
This study demonstrated that ethanol promoted RANKL-induced osteoclast formation and bone resorption, whereas, disulfiram suppressed ethanol-induced fractures by abrogating the expression of nuclear factor of activated T cell c1 (NFATc1) in vitro.
Ethanol Impairs Estrogen Receptor Signaling Resulting in Accelerated Activation of Senescence Pathways, Whereas Estradiol Attenuates the Effects of Ethanol in Osteoblasts
TLDR
It is concluded 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.
Phosphate enhances reactive oxygen species production and suppresses osteoblastic differentiation
TLDR
The results indicate that phosphate suppresses osteoblastic differentiation at least in part by enhancing ROS production in MC3T3-E1 cells.
High glucose potentiates collagen synthesis and bone morphogenetic protein-2-induced early osteoblast gene expression in rat spinal ligament cells.
TLDR
High glucose, via production of reactive oxygen species, subsequent activation of PKC, and inhibition of p38, enhances type I collagen synthesis and expression of early osteogenesis genes induced by BMP-2 in rat spinal ligament cells.
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References

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Estradiol Protects against Ethanol-Induced Bone Loss by Inhibiting Up-Regulation of Receptor Activator of Nuclear Factor-κB Ligand in Osteoblasts
TLDR
E2 prevents EtOH-induced bone loss by opposing the induction of RANKL mRNA in osteoblasts and ethanol-induced osteoclastogenesis, through opposing effects on sustained ERK signaling.
Reactive Oxygen Species Stimulates Receptor Activator of NF-κB Ligand Expression in Osteoblast*
  • X. Bai, Di Lu, +6 authors S. Luo
  • Biology, Medicine
    Journal of Biological Chemistry
  • 2005
TLDR
Increased intracellular ROS levels by H2O2 or xanthine/xanthine oxidase-generated superoxide anion stimulated RANKL mRNA and protein expression in human osteoblast-like MG63 cell line and primary mouse bone marrow stromal cells and calvarial osteoblasts and via ERKs and HSF2 in human MG63 cells.
A crucial role for thiol antioxidants in estrogen-deficiency bone loss.
TLDR
Observations strongly suggest that estrogen deficiency causes bone loss by lowering thiol antioxidants in osteoclasts, which directly sensitizes osteoclast to osteoclastogenic signals and entrains ROS-enhanced expression of cytokines that promote osteoclastic bone resorption.
STAT3 Activation in Stromal/Osteoblastic Cells Is Required for Induction of the Receptor Activator of NF-κB Ligand and Stimulation of Osteoclastogenesis by gp130-utilizing Cytokines or Interleukin-1 but Not 1,25-Dihydroxyvitamin D3 or Parathyroid Hormone*
TLDR
It is demonstrated that activation of the gp130-STAT3 pathway in stromal/osteoblastic cells mediates the osteoclastogenic effects of IL-1, but not parathyroid hormone or 1,25-dihydroxyvitamin D3.
Chronic alcohol ingestion induces osteoclastogenesis and bone loss through IL-6 in mice.
TLDR
It is demonstrated that ethanol induces bone loss through IL-6 and it is suggested that IL- 6 achieves this effect by inducing RANKL and promoting CFU-GM formation and osteoclastogenesis.
Involvement of reactive oxygen species in cardiotrophin-1-induced proliferation of cardiomyocytes differentiated from murine embryonic stem cells.
TLDR
It is concluded that CT-1 stimulates the proliferation of ES cell-derived cardiomyocytes by signaling pathways that involve ROS as signaling molecules in the signal transduction cascade.
Transient Versus Sustained Phosphorylation and Nuclear Accumulation of ERKs Underlie Anti-Versus Pro-apoptotic Effects of Estrogens*
TLDR
Findings indicate that the kinetics of ERK phosphorylation and the length of time that phospho-ERKs are retained in the nucleus are responsible for pro-versus anti-apoptotic effects of estrogen on different cell types of bone and perhaps their many other target tissues.
Chronic ethanol feeding increases activation of NADPH oxidase by lipopolysaccharide in rat Kupffer cells: role of increased reactive oxygen in LPS‐stimulated ERK1/2 activation and TNF‐α production
TLDR
It is demonstrated that chronic ethanol feeding increases LPS‐stimulated NADPH oxidase‐dependent production of ROS in Kupffer cells, contributing to enhanced LPS-stimulated TNF‐α production by K upffer cells after chronic ethanol Feeding.
17β-Estradiol inhibits NADPH oxidase activity through the regulation of p47phox mRNA and protein expression in THP-1 cells
In this report, we demonstrate that NADPH oxidase is activated by tumor necrosis factor-alpha (TNF-alpha) plus interferon-gamma (IFN-gamma) in human monocytic cells (THP-1 cells) differentiated with
17beta-estradiol inhibits NADPH oxidase activity through the regulation of p47phox mRNA and protein expression in THP-1 cells.
TLDR
It is implicate that 17beta-estradiol has an anti-atherosclerotic effects through the improvement of nitric oxide (NO) bioavailability caused by the regulation of superoxide (O(2)(-)) production.
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