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Fibroblast Growth Factor 2 Promotes Bladder Hypertrophy Caused by Partial Bladder Outlet Obstruction
Ye Gao1, Peilin Liu1, Fan He1
1Department of Urology, Second Affiliated Hospital, Army Medical University, Chongqing, China.
Frontiers in Cell and Developmental Biology
|April 16, 2021
Summary
Identifying non-invasive biomarkers for bladder outlet obstruction (BOO) is crucial. Fibroblast growth factor 2 (FGF2) shows potential, correlating with prostate volume in benign prostatic hyperplasia (BPH) patients.
Area of Science:
- Urology
- Biochemistry
- Molecular Biology
Background:
- Non-invasive biomarkers are needed to diagnose bladder outlet obstruction (BOO)-related dysfunction.
- Current diagnostic methods for BOO lack non-invasive molecular markers.
Purpose of the Study:
- To investigate molecular changes and identify biomarkers associated with partial BOO (PBOO).
- To explore the role of fibroblast growth factor 2 (FGF2) and brain-derived neurotrophic factor (BDNF) in PBOO and benign prostatic hyperplasia (BPH).
Main Methods:
- Established a PBOO rat model.
- Utilized RNA sequencing, TMT-labeling proteomics, ELISA, and immunohistochemistry.
- Analyzed serum samples from 60 BPH patients.
Main Results:
- PBOO induced smooth muscle hypertrophy and interstitial cell hyperplasia in rats within 4 weeks.
- After 4 weeks, PBOO led to immune response activation, cell death, and apoptosis.
- FGF2 levels correlated with prostate volume in BPH patients, suggesting its involvement in hypertrophy.
Conclusions:
- Bladder function shifts from compensation to decompensation at 4 weeks post-PBOO.
- FGF2 is implicated in PBOO bladder hypertrophy and correlates with prostate volume in BPH.
- Further research into FGF2 as a biomarker for BOO and BPH is warranted.
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