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Radiation-induced apoptosis in microvascular endothelial cells
R E Langley1, E A Bump, S G Quartuccio
1Joint Center for Radiation Therapy, Harvard Medical School and Dana-Farber Cancer Institute, Boston, MA 02115, USA.
British Journal of Cancer
|January 1, 1997
Summary
Basic fibroblast growth factor (bFGF) withdrawal or ionizing radiation induces apoptosis in capillary endothelial cells. Radiation-induced apoptosis is worsened when bFGF is absent, highlighting bFGF's protective role.
Area of Science:
- Cell Biology
- Radiation Biology
- Oncology
Background:
- The microvasculature's response to ionizing radiation impacts normal tissue and tumor outcomes.
- Basic fibroblast growth factor (bFGF) protects large vessel endothelial cells from radiation-induced apoptosis.
- Capillary endothelial cells (ECs) differ phenotypically from large vessel cells.
Purpose of the Study:
- To investigate the apoptotic response of capillary endothelial cells (ECs) to ionizing radiation and bFGF.
- To determine if bFGF influences radiation-induced apoptosis in microvessel ECs.
Main Methods:
- Assessed apoptosis via nuclear morphology changes, cell detachment rates, and DNA fragmentation.
- Exposed confluent EC monolayers to ionizing radiation (2-10 Gy) with and without bFGF.
- Varied the duration of bFGF withdrawal to assess its impact on apoptosis.
Main Results:
- bFGF withdrawal alone induced apoptosis in EC monolayers, dependent on withdrawal duration.
- Ionizing radiation triggered dose-dependent apoptosis in ECs, peaking 6-10 hours post-irradiation.
- Radiation-induced apoptosis was significantly enhanced (e.g., 44.3% vs. 19.8% at 10 Gy) in ECs deprived of bFGF.
Conclusions:
- Both bFGF withdrawal and ionizing radiation can independently induce apoptosis in capillary endothelial cells.
- The presence of bFGF modifies and potentially mitigates radiation-induced apoptosis in microvessel ECs.