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Increased radiosensitivity and radiation-induced apoptosis in SRC-3 knockout mice
1Institute of Combined Injury, State Key Laboratory of Trauma, Burns and Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Third Military Medical University, Chongqing 400038, China.
Journal of Radiation Research
|December 7, 2013
Summary
Steroid receptor coactivator-3 (SRC-3) deficiency increases radiation-induced apoptosis in hematopoietic cells, leading to higher mortality. This suggests SRC-3 regulates radiosensitivity and may be a therapeutic target for radiation injury.
Area of Science:
- Molecular Biology
- Hematology
- Radiation Oncology
Background:
- Steroid receptor coactivator-3 (SRC-3) is a transcriptional coactivator involved in chemoresistance.
- The role of SRC-3 in radiation-induced apoptosis in hematopoietic cells remains largely unknown.
Purpose of the Study:
- To investigate the role of SRC-3 in radiation-induced hematopoietic injury using SRC-3 knockout mice.
- To determine SRC-3's impact on the radiosensitivity of bone marrow hematopoietic cells.
Main Methods:
- Utilized SRC-3 knockout (SRC-3(-/-)) mice and wildtype littermates.
- Administered a range of irradiation doses to assess in vivo hematopoietic injury.
- Quantified peripheral blood cell counts, bone marrow mononuclear cells, and apoptosis rates.
Main Results:
- SRC-3(-/-) mice showed significantly reduced peripheral blood and bone marrow cellularity post-irradiation.
- Bone marrow depression was more severe in SRC-3(-/-) mice, resulting in higher mortality.
- Bone marrow mononuclear cells from SRC-3(-/-) mice exhibited increased radiation-induced apoptosis.
Conclusions:
- SRC-3 plays a critical role in protecting bone marrow hematopoietic cells from radiation-induced apoptosis.
- Modulating SRC-3 expression could impact hematopoietic cell radiosensitivity.
- SRC-3 represents a potential therapeutic target for mitigating radiation-induced hematopoietic injury.
