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Anabolic steroids reduce spinal cord injury-related bone loss in rats associated with increased Wnt signaling
Li Sun1, Jiangping Pan2, Yuanzhen Peng1
1Mount Sinai Bone Program, Mount Sinai School of Medicine, New York, NY, USA.
Background:
Spinal cord injury (SCI) causes severe bone loss. At present, there is no practical treatment to delay or prevent bone loss in individuals with motor-complete SCI. Hypogonadism is common in men after SCI and may exacerbate bone loss. The anabolic steroid nandrolone reduces bone loss due to microgravity or nerve transection.
Objective:
To determine whether nandrolone reduced bone loss after SCI and, if so, to explore the mechanisms of nandrolone action.
Methods:
Male rats with complete transection of the spinal cord were administered nandrolone combined with a physiological replacement dose of testosterone, or vehicle, beginning on day 29 after SCI and continued for 28 days.
Results:
SCI reduced distal femoral and proximal tibial bone mineral density (BMD) by 25 and 16%, respectively, at 56 days. This bone loss was attenuated by nandrolone. In ex vivo osteoclasts cultures, SCI increased mRNA levels for tartrate-resistant acid phosphatase (TRAP) and calcitonin receptor; nandrolone-normalized expression levels of these transcripts. In ex vivo osteoblast cultures, SCI increased receptor activator of NF-kB ligand (RANKL) mRNA levels but did not alter osteoprotegerin (OPG) mRNA expression; nandrolone-increased expression of OPG and OPG/RANKL ratio. SCI reduced mRNA levels of Wnt signaling-related genes Wnt3a, low-density lipoprotein receptor-related protein 5 (LRP5), Fzd5, Tcf7, and ectodermal-neural cortex 1 (ENC1) in osteoblasts, whereas nandrolone increased expression of each of these genes.
Conclusions:
The results demonstrate that nandrolone reduces bone loss after SCI. A potential mechanism is suggested by our findings wherein nandrolone modulates genes for differentiation and activity of osteoclasts and osteoblasts, at least in part, through the activation of Wnt signaling.
Insights
Nandrolone effectively reduces bone loss following spinal cord injury (SCI) in rats. It works by modulating genes involved in osteoclast and osteoblast activity, potentially through Wnt signaling activation.
Area of Science:
- Orthopedics and Rehabilitation
- Endocrinology
- Cell Biology
Background:
- Spinal cord injury (SCI) leads to significant bone loss, with no current effective treatments for motor-complete injuries.
- Hypogonadism is common post-SCI and can worsen bone density loss.
- Nandrolone, an anabolic steroid, has shown potential in mitigating bone loss from other conditions.
Purpose of the Study:
- To investigate if nandrolone can reduce bone loss after SCI in a rat model.
- To explore the underlying molecular mechanisms by which nandrolone exerts its effects on bone metabolism post-SCI.
Main Methods:
- Male rats underwent spinal cord transection (SCI) and were treated with nandrolone and testosterone or vehicle.
- Bone mineral density (BMD) was measured at distal femur and proximal tibia.
- Gene expression analysis was performed on ex vivo osteoclast and osteoblast cultures.
Main Results:
- SCI caused significant bone loss (25% femur, 16% tibia), which was attenuated by nandrolone.
- Nandrolone normalized osteoclast-related gene expression (TRAP, calcitonin receptor) and increased osteoblast OPG/RANKL ratio.
- Nandrolone upregulated Wnt signaling pathway genes (Wnt3a, LRP5, Fzd5, Tcf7, ENC1) in osteoblasts.
Conclusions:
- Nandrolone demonstrates efficacy in reducing bone loss post-SCI.
- The mechanism involves modulating osteoclast and osteoblast gene expression, potentially via Wnt signaling activation.
