Progressive slowdown/prevention of cellular senescence by CD9-targeted delivery of rapamycin using lactose-wrapped calcium carbonate nanoparticles
Open accessAbstract
Cellular senescence, a state of irreversible growth arrest and altered cell function, causes aging-related diseases. Hence, treatment modalities that could target aging cells would provide a robust therapeutic avenue. Herein, for the first time, we utilized CD9 receptors (overexpressed in senescent cells) for nanoparticle targeting in addition to the inherent β-galactosidase activity. In our study, CD9 monoclonal antibody-conjugated lactose-wrapped calcium carbonate nanoparticles loaded with rapamycin (CD9-Lac/CaCO 3/Rapa) were prepared for targeted rapamycin delivery to senescent cells. The nanoparticles exhibited an appropriate particle size (~130 nm) with high drug-loading capacity (~20%). In vitro drug release was enhanced in the presence of β-galactosidase suggesting potential cargo drug delivery to the senescent cells. Furthermore, CD9-Lac/CaCO 3/Rapa exhibited high uptake and anti-senescence effects (reduced β-galactosidase and p53/p21/CD9/cyclin D1 expression, reduced population doubling time, enhanced cell proliferation and migration, and prevention of cell cycle arrest) in old human dermal fibroblasts. Importantly, CD9-Lac/CaCO 3/Rapa significantly improved the proliferation capability of old cells as suggested by BrdU staining along with significant reductions in senescence-associated secretory phenotypes (IL-6 and IL-1β) (P < 0.05). Altogether, our findings suggest the potential applicability of CD9-Lac/CaCO 3/Rapa in targeted treatment of senescence.
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Rapamycin and its analogue RAD001 reduced the protumorigenic SASP, prevented senescence, impaired SASP-mediated immune recognition of oncogene-expressing cells, and improved liver dysfunction in naturally aged mice.
“Treatment with rapamycin (and its analogue RAD001)232 attenuated the protumorigenic SASP230, prevented senescence233, impaired SASP-mediated immune recognition of oncogene-expressing cells and ameliorated liver dysfunction in naturally aged mice231.”
From Cellular senescence in ageing: from mechanisms to therapeutic opportunities (2021) · cites this paper as [233]
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- Authors
- Thapa, R. K., Nguyen, H. T., Jeong, J.-H., Kim, J. R., Choi, H.-G., Yong, C. S., & Kim, J. O.
- Affiliations
- Yeungnam University (KR)
- Yeungnam University College (KR)
- Hanyang University (KR)
- Corresponding author
- Kim, Jae Ryong
- Yong, Chul Soon
- Kim, Jong Oh
- ORCID
- Venue
- Scientific Reports
- Published
- 2017-04-10
- Volume
- 7
- Issue
- 1
- Pages
- 43299-43299
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC5385881
- OpenAlex
- W2605847570
- Cited by
- 115
- References
- 39
- Citations by year
- 2026: 6 · 2025: 15 · 2024: 21 · 2023: 10 · 2022: 19 · 2021: 9 · 2020: 14 · 2019: 9 · 2018: 8 · 2017: 4
- FWCI
- 3.45
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Research Foundation (2015R1A5A2009124)
- Ministry of Science, ICT and Future Planning (2015R1A2A2A01004118, 2015R1A2A2A04004806, 2015R1A5A2009124)
- National Research Foundation of Korea (2015R1A2A2A01004118, 2015R1A2A2A04004806, 2015R1A5A2 009124, 2015R1A2A2A01004118, 2015R1A2A2A04004806)
- Topics
- Physical Sciences › Materials Science › Biomaterials › Nanoparticle-Based Drug Delivery
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA Interference and Gene Delivery
- Keywords
- cellular senescence, rapamycin, calcium carbonate nanoparticles, targeted drug delivery, beta-galactosidase, dermal fibroblasts, aging, senescence-associated secretory phenotype, cell proliferation, anti-senescence therapy
- MeSH terms
- Antibodies, Monoclonal, Calcium Carbonate, Cells, Cultured, Fibroblasts, Humans, Lactose, Cellular Senescence, Sirolimus, Cell Proliferation, Nanoparticles, Tetraspanin 29
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