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Basic Fibroblast Growth Factor Ameliorates Endothelial Dysfunction in Radiation-Induced Bladder Injury.
Shiwei Zhang1, Xuefeng Qiu2, Yanting Zhang3
1Department of Urology, Affiliated Drum Tower Hospital, School of Medicine, Nanjing University, Nanjing 210008, China ; Institute of Urology, Nanjing University, Nanjing 210008, China ; Department of Surgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210002, China.
Basic fibroblast growth factor (bFGF) treatment improved radiation-induced endothelial dysfunction in the urinary bladder. bFGF preserved bladder histology by reducing inflammation and fibrosis in radiation-induced bladder injury.
Area of Science:
- Oncology
- Radiology
- Cell Biology
Background:
- Radiation therapy often causes urinary bladder injury, leading to endothelial dysfunction and histological damage.
- Radiation-induced bladder injury (RIBI) is characterized by reduced thrombomodulin (TM) expression and increased apoptosis.
- Endothelial dysfunction is a key feature of RIBI, impacting bladder tissue integrity.
Purpose of the Study:
- To investigate the therapeutic potential of basic fibroblast growth factor (bFGF) in mitigating radiation-induced endothelial dysfunction and histological changes in the urinary bladder.
- To evaluate the effect of bFGF on thrombomodulin (TM) expression and apoptosis in radiation-exposed human umbilical vein cells (HUVEC) and urinary bladder tissue.
- To assess bFGF's efficacy in preserving bladder histology during both early and delayed phases of radiation-induced bladder injury (RIBI).
Main Methods:
- Administration of bFGF to HUVEC and urinary bladder tissue immediately following radiation exposure.
- Assessment of thrombomodulin (TM) expression in HUVEC and urinary bladder tissue post-radiation and bFGF treatment.
- Evaluation of apoptosis in HUVEC and histological changes (urothelium thickness, inflammation, fibrosis) in the urinary bladder at early and delayed time points.
Main Results:
- Radiation exposure reduced TM expression and increased apoptosis in HUVEC and urinary bladder.
- bFGF administration increased TM expression in HUVEC and urinary bladder tissue.
- bFGF treatment reduced apoptosis in HUVEC, increased urothelium thickness, decreased inflammation in the early phase, and reduced fibrosis in the delayed phase of RIBI.
Conclusions:
- Endothelial dysfunction is a significant component of radiation-induced bladder injury.
- bFGF effectively ameliorates radiation-induced endothelial dysfunction in the urinary bladder.
- bFGF administration preserves urinary bladder histology by mitigating early and delayed radiation-induced damage, offering a potential therapeutic strategy.
