Mitigation of ionizing radiation-induced bone marrow suppression by p38 inhibition and G-CSF administration.
Open accessAbstract
p38 mitogen-activated protein kinases (p38) has been shown to be activated in hematopoietic stem and progenitors cells after exposure to ionizing radiation (IR) and its activation has been implicated in bone marrow (BM) suppression under various pathological conditions. Therefore, in the present study we investigated whether inhibition of p38 activity alone with SB203580 (SB, a specific p38 inhibitor) or in combination with granulocyte colony-stimulating factor (G-CSF) can mitigate total body irradiation (TBI)-induced BM damage and lethality. Our results showed that p38 inhibition with SB had no significant effect on the 30-day survival rates of the mice exposed to 7.2 Gy TBI when it was used alone but increased the survival of the mice when it was combined with G-CSF. This combined effect may be attributable to a better preservation or stimulation of hematopoietic stem and progenitor cells, because BM cells from SB and G-CSF-treated mice produced more colony forming units-granulocyte-macrophage (CFU-GM) and 4-week cobblestone area forming cells (CAFCs) than the cells from either SB or G-CSF-treated mice after TBI in a colony forming cell assay and a CAFC assay, respectively. These findings suggest that the combined therapy with SB and G-GSF is more effective in mitigating TBI-induced acute BM injury than either agent alone.
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Activation of p38 was involved in IR-induced BM hematopoietic cell senescence and dysfunction.
“activation of p38 was involved in IR-induced BM hematopoietic cell senescence and dysfunction.30,40”
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 [40]
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- Authors
- LI, D., WANG, Y., WU, H., LU, L., ZHANG, H., CHANG, J., ZHAI, Z., ZHANG, J., WANG, Y., ZHOU, D., & MENG, A.
- Affiliations
- Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
- Medical University of South Carolina (US)
- University of Arkansas for Medical Sciences (US)
- Corresponding author
- MENG, Aimin
- ORCID
- Venue
- Journal of Radiation Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2011
- Volume
- 52
- Issue
- 6
- Pages
- 712-716
- ISSN
- 0449-3060 (ISSN-L)
- 1349-9157
- PMC
- PMC3390190
- OpenAlex
- W2054899210
- Cited by
- 28
- References
- 36
- Citations by year
- 2026: 1 · 2025: 1 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 1 · 2016: 4 · 2015: 2 · 2014: 5 · 2013: 5
- FWCI
- 2.44
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Journal of Radiation Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Natural Science Foundation of China (973 Program)
- National Key Research and Development Program of China (2011CB964800)
- 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 › Hematology › Acute Myeloid Leukemia Research
- Keywords
- p38 MAPK inhibition, SB203580, granulocyte colony-stimulating factor, total body irradiation, hematopoietic stem and progenitor cells, hematopoietic recovery, cobblestone area-forming cells, CFU-GM, radiation lethality, combination therapy
- MeSH terms
- Animals, Bone Marrow, Colony-Forming Units Assay, Gamma Rays, Imidazoles, Male, Mice, Inbred C57BL, Pyridines, Recombinant Proteins, Whole-Body Irradiation, Granulocyte Colony-Stimulating Factor, Protein Kinase Inhibitors, p38 Mitogen-Activated Protein Kinases, Mice
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