Skeletal Response to Soluble Activin Receptor Type IIB in Mouse Models of Osteogenesis Imperfecta
Open accessAbstract
Osteogenesis imperfecta (OI) is a heritable connective tissue disorder primarily due to mutations in the type I collagen genes (COL1A1 and COL1A2), leading to compromised biomechanical integrity in type I collagen-containing tissues such as bone. Bone is inherently mechanosensitive and thus responds and adapts to external stimuli, such as muscle mass and contractile strength, to alter its mass and shape. Myostatin, a member of the TGF-β superfamily, signals through activin receptor type IIB to negatively regulate muscle fiber growth. Because of the positive impact of myostatin deficiency on bone mass, we utilized a soluble activin receptor type IIB-mFc (sActRIIB-mFc) fusion protein in two molecularly distinct OI mouse models (G610C and oim) and evaluated their bone properties. Wild-type (WT), +/G610C, and oim/oim mice were treated from 2 to 4 months of age with either vehicle (Tris-buffered saline) or sActRIIB-mFc (10 mg/kg). Femurs of sActRIIB-mFc-treated mice exhibited increased trabecular bone volume regardless of genotype, whereas the cortical bone microarchitecture and biomechanical strength were only improved in WT and +/G610C mice. Dynamic histomorphometric analyses suggest the improved cortical bone geometry and biomechanical integrity reflect an anabolic effect due to increased mineral apposition and bone formation rates, whereas static histomorphometric analyses supported sActRIIB-mFc treatment also having an anti-catabolic impact with decreased osteoclast number per bone surface on trabecular bone regardless of sex and genotype. Together, our data suggest that sActRIIB-mFc may provide a new therapeutic direction to improve both bone and muscle properties in OI. © 2018 American Society for Bone and Mineral Research.
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The ACVR2B/Fc strategy has been shown to be effective in a mouse model of osteogenesis imperfecta, which is characterized by both muscle atrophy and bone fragility.
“The dual ability of ACVR2B/Fc to promote muscle growth and to increase bone density has suggested the possibility that this therapeutic strategy may be particularly useful to combat simultaneously comorbid muscle and bone loss, and indeed, this strategy has been shown to be effective in a mouse model of osteogenesis imperfecta, which is characterized by both muscle atrophy and bone fragility (21,”
From Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight (2020) · cites this paper as [22]
The Results report increased skeletal muscle mass with sActRIIB-mFc treatment, and the Discussion reports improved trabecular bone architecture in both OI mouse models. The paper documents bone fragility, but the passages found do not establish that these models are characterized by muscle atrophy; it also reports no reduction in fracture occurrence. (LLM, conf=0.82)
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Targeting myostatin/activin A protects against skeletal muscle and bone loss during spaceflight
Lee, S.-J., Lehar, A., Meir, J. U., Koch, C., Morgan, A., Warren, L. E., Rydzik, R., Youngstrom, D. W., Chandok, H., George, J., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2014716117 · Cited by 115 · see citing works
“The dual ability of ACVR2B/Fc to promote muscle growth and to increase bone density has suggested the possibility that this therapeutic strategy may be particularly useful to combat simultaneously comorbid muscle and bone loss, and indeed, this strategy has been shown to be effective in a mouse model of osteogenesis i…”
Myostatin/Activin Receptor Ligands in Muscle and the Development Status of Attenuating Drugs
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- Authors
- Jeong, Y., Daghlas, S. A., Xie, Y., Hulbert, M. A., Pfeiffer, F. M., Dallas, M. R., Omosule, C. L., Pearsall, R. S., Dallas, S. L., & Phillips, C. L.
- Affiliations
- University of Missouri (US)
- University of Missouri–Kansas City (US)
- Acceleron Pharma (United States) (US)
- Corresponding author
- Phillips, Charlotte L
- ORCID
- Venue
- Journal of Bone and Mineral Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-05-29
- Volume
- 33
- Issue
- 10
- Pages
- 1760-1772
- ISSN
- 0884-0431 (ISSN-L)
- 1523-4681
- PMC
- PMC6400483
- OpenAlex
- W2805139743
- Cited by
- 36
- References
- 61
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 1 · 2022: 3 · 2021: 13 · 2020: 5 · 2019: 3
- FWCI
- 3.21
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Journal of Bone and Mineral Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Aeronautics and Space Administration
- March of Dimes Foundation
- University of Missouri
- National Institutes of Health (AG039355)
- National Institute on Aging (P01AG039355)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR055907, R21AR062346)
- Office of Experimental Program to Stimulate Competitive Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Connective tissue disorders research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone health and osteoporosis research
- Keywords
- osteogenesis imperfecta, myostatin, type I collagen, COL1A1, COL1A2, trabecular bone volume, cortical bone microarchitecture, bone strength, bone formation, osteoclasts, bone remodeling, TGF-beta superfamily, muscle-bone crosstalk
- MeSH terms
- Animals, Biomechanical Phenomena, Bone and Bones, Disease Models, Animal, Female, Femur, Male, Mice, Inbred C57BL, Osteoblasts, Osteoclasts, Osteocytes, Osteogenesis Imperfecta, Peptide Fragments, Procollagen, Recombinant Fusion Proteins, Solubility, Biomarkers, Activin Receptors, Type II, Torsion, Mechanical
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