An Influence of Anti-Sclerostin Oligonucleotide Aptamers on Viability and Proliferation of Osteoblasts and Osteoclasts in vitro
Osteoporosis is a metabolic skeletal disease characterized by a high risk of fractures with minimal trauma due to decreased bone mass, microarchitecture, bone mineralization, and bone strength. The range of drugs for the treatment of osteoporosis is limited, and patients often have certain restrictions on their use. It is important to search for new therapeutic options for the treatment of osteoporosis. The leading role of the Wnt pathway in the process of bone remodeling has been proven. Oligonucleotide aptamers represent promising alternative to antibodies for targeted regulation of Wnt pathway, particularly through an inhibition of functional activity of Wnt antagonist sclerostin. In this study, we produced a series of chemically modified DNA aptamers targeting sclerostin and assessed their properties by in vitro experiments with osteoblasts and osteoclasts. We conducted that aptamers do not have cytotoxicity against osteoblasts and osteoclasts. Based on these results, aptamers are promising for further investigation of their targeting interactions with Wnt-pathway inhibitors.
Authors
- V. O. Omelchenko (ORCID: https://orcid.org/0000-0001-6606-7185)
- Natalya A. Sitnikova (ORCID: https://orcid.org/0000-0002-8226-8996)
- Nadezhda O. Kropacheva
- Natalya Bondarenko (ORCID: https://orcid.org/0000-0002-1291-8527)
- Mariya Vorobyeva (ORCID: https://orcid.org/0000-0001-5317-3288)
- М. А. Королев (ORCID: https://orcid.org/0000-0002-4890-0847)
Institutions
- Russian Academy of Sciences (RU)
- Institute of Chemical Biology and Fundamental Medicine (RU)
- Institute of Cytology and Genetics (RU)
- Siberian Branch of the Russian Academy of Sciences (RU)
- Institute of Clinical and Experimental Lymphology (RU)
Publication Details
- Published
- 2024-09-30
- DOI
- https://doi.org/10.1109/sibircon63777.2024.10758523
- Primary Topic
- RNA Interference and Gene Delivery
- Type
- article
- Field-Weighted Citation Impact
- 0.00