Hyperglycemia Accelerated Endothelial Progenitor Cell Senescence via the Activation of p38 Mitogen-Activated Protein Kinase
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BACKGROUND: Both the number and function of bone marrow-derived endothelial progenitor cells (EPCs) have been shown to be impaired in patients with diabetes mellitus. Therefore, we investigated the effect of glucose on the senescence of EPCs. METHODS AND RESULTS: EPCs were isolated from human peripheral blood and characterized to evaluate the effect of glucose (in 5-12.5 mmol/L) on the rate of senescence by acidic beta-galactosidase staining. The phosphorylation of p38 mitogen-activated protein kinase (MAPK) level was analyzed by ELISA. The exposure of cultured EPC to high glucose (HG; 12.5 mmol/L) significantly accelerated the rate of senescence compared with that in osmolar control (L-glucose) during 10 days culture. An inhibitory effect of HG on EPC proliferation disclosed by an MTS assay. The phosphorylation of p38 MAPK in EPCs was also increased by glucose compared with control in a dose-dependent manner. HG-induced EPC senescence was significantly inhibited by the addition of an inhibitor of the p38 MAPK, SB203580. CONCLUSIONS: HG accelerates the onset of EPCs senescence leading to the impairment of proliferative activity, which might be related to the phosphorylation of p38 MAPK.
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Elevated glucose and lipid levels themselves, like inflammation, can induce cellular senescence.
“For example, elevated glucose and lipid levels themselves, like inflammation, can induce cellular senescence [11, 37].”
From Cellular senescence: at the nexus between ageing and diabetes (2019) · cites this paper as [37]
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- Authors
- Kuki, S., Imanishi, T., Kobayashi, K., Matsuo, Y., Obana, M., & Akasaka, T.
- Affiliations
- Wakayama Medical University (JP)
- Venue
- Circulation Journal
- Publisher
- Japanese Circulation Society
- Published
- 2006
- Volume
- 70
- Issue
- 8
- Pages
- 1076-1081
- ISSN
- 1346-9843 (ISSN-L)
- 1347-4820
- OpenAlex
- W2067349642
- Cited by
- 137
- References
- 41
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 2 · 2023: 4 · 2022: 9 · 2021: 11 · 2020: 2 · 2019: 3 · 2018: 4 · 2017: 8 · 2016: 6 · 2015: 7 · 2014: 5 · 2013: 6 · 2012: 7
- FWCI
- 6.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Journal (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Angiogenesis and VEGF in Cancer
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- endothelial progenitor cells, hyperglycemia, cellular senescence, p38 MAPK, diabetes mellitus, high glucose, cell proliferation, SB203580, beta-galactosidase staining
- MeSH terms
- Cell Differentiation, Cells, Cultured, Dose-Response Relationship, Drug, Enzyme Activation, Enzyme Inhibitors, Glucose, Humans, Hyperglycemia, Imidazoles, Mitosis, Phosphorylation, Pyridines, Stem Cells, Signal Transduction, Cellular Senescence, Endothelial Cells, p38 Mitogen-Activated Protein Kinases, Cell Proliferation
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