Mn(III) meso-tetrakis-(N-ethylpyridinium-2-yl) porphyrin mitigates total body irradiation-induced long-term bone marrow suppression.
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Our recent studies showed that total body irradiation (TBI) induces long-term bone marrow (BM) suppression in part by induction of hematopoietic stem cell (HSC) senescence through reactive oxygen species (ROS). In this study, we examined if Mn(III) meso-tetrakis-(N-ethylpyridinium-2-yl) porphyrin (MnTE), a superoxide dismutase mimetic and potent antioxidant, can mitigate TBI-induced long-term BM injury in a mouse model. Our results showed that post-TBI treatment with MnTE significantly inhibited the increases in ROS production and DNA damage in HSCs and the reduction in HSC frequency and clonogenic function induced by TBI. In fact, the clonogenic function of HSCs from irradiated mice after MnTE treatment was comparable to that of HSCs from normal controls on a per-HSC basis, suggesting that MnTE treatment inhibited the induction of HSC senescence by TBI. This suggestion is supported by the finding that MnTE treatment also reduced the expression of p16(Ink4a) (p16) mRNA in HSCs induced by TBI and improved the long-term and multilineage engraftment of irradiated HSCs after transplantation. Therefore, the results from this study demonstrate that MnTE has the potential to be used as a therapeutic agent to mitigate TBI-induced long-term BM suppression by inhibiting ionizing radiation-induced HSC senescence through the ROS-p16 pathway.
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Previous studies suggest that IR induces HSC senescence primarily via induction of oxidative stress.
“Our previous studies suggest that IR induces HSC senescence primarily via induction of oxidative stress,9,23,30”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [9]
Treating irradiated mice with various antioxidants after IR significantly attenuated TBI-induced LSK cell senescence and residual BM suppression.
“Treating the irradiated mice with various antioxidants after IR significantly attenuated TBI-induced LSK cell senescence and residual BM suppression.9,30”
From Total body irradiation causes long-term mouse BM injury via induction of HSC premature senescence in an Ink4a- and Arf-independent manner (2014) · cites this paper as [9]
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- Authors
- Li, H., Wang, Y., Pazhanisamy, S. K., Shao, L., Batinic-Haberle, I., Meng, A., & Zhou, D.
- Affiliations
- Medical University of South Carolina (US)
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Corresponding author
- Zhou, Daohong
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-07
- Volume
- 51
- Issue
- 1
- Pages
- 30-37
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3390209
- OpenAlex
- W2058302375
- Cited by
- 68
- References
- 46
- Citations by year
- 2025: 3 · 2024: 1 · 2023: 2 · 2022: 2 · 2021: 2 · 2020: 2 · 2019: 9 · 2018: 6 · 2017: 6 · 2016: 3 · 2015: 10 · 2014: 7 · 2013: 7 · 2012: 5
- FWCI
- 5.38
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Medical University of South Carolina
- National Cancer Institute (R01CA122023, R01CA086860)
- National Institute of Allergy and Infectious Diseases (R01AI080421)
- Topics
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Effects of Radiation Exposure
- Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
- Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
- Keywords
- MnTe, total body irradiation, myelosuppression, reactive oxygen species, p16INK4a, superoxide dismutase mimetic, antioxidants, DNA damage, engraftment
- MeSH terms
- Animals, Antioxidants, Bone Marrow, Flow Cytometry, Hematopoietic Stem Cells, Male, Metalloporphyrins, Mice, Inbred C57BL, Whole-Body Irradiation, Bone Marrow Transplantation, Cellular Senescence, Reactive Oxygen Species, Oxidative Stress, Cyclin-Dependent Kinase Inhibitor p16, Mice
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