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Evaluation of PGP 9.5, NGFR, TGFβ1, FGFR1, MMP-2, AT2R2, SHH, and TUNEL in Primary Obstructive Megaureter Tissue
Anna Junga1, Ivo Siņicins1, Aigars Pētersons2
1Institute of Anatomy and Anthropology, Riga Stradins University, Riga, Latvia.
Abstract:
Primary obstructive megaureter (POM) morphogenesis is not fully known. The aim of the study was to evaluate the appearance of different factors that might take part in the pathogenesis of POM. Megaureter tissues of 14 children were stained with hematoxylin and eosin as well as with immunohistochemistry for protein gene product 9.5, nerve growth factor receptor, transforming growth factor beta 1 (TGFβ1), fibroblast growth factor receptor 1 (FGFR1), matrix metalloproteinase 2 (MMP-2), angiotensin 2 receptor type 2, and sonic hedgehog (SHH) protein. Apoptosis was detected by terminal dUTP nick-end labeling reaction. POM tissues revealed transitional epithelium with scattered vacuolization, submucosa with inflammatory cells, and focally vacuolized and chaotically organized muscle layers. Apoptosis, appearance of MMP-2, FGFR1, and SHH prevailed, but TGFβ1 positive cell number was lower in patients. Correlation between MMP-2 in epithelium and endothelium, FGFR1 and MMP-2 in epithelium, and TGFβ1 in epithelium and connective tissue in patients was detected. POM morphopathogenesis involves an apoptotic cell death of epithelium and smooth muscle as well as tissue degradation in epithelium and connective tissue of the ureter wall. The decrease of tissue growth through diminished TGFβ1 expression and stimulation of FGFR1 and MMP-2 suggests a disbalance of tissue remodelation in the megaureter wall.
Insights
Primary obstructive megaureter (POM) involves increased apoptosis and tissue degradation. Factors like FGFR1 and MMP-2 are elevated, while TGFβ1 is decreased, indicating a remodeling imbalance.
Area of Science:
- Urology
- Developmental Biology
- Pathology
Background:
- The precise mechanisms underlying primary obstructive megaureter (POM) development remain unclear.
- Understanding POM pathogenesis is crucial for effective diagnosis and treatment strategies.
Purpose of the Study:
- To investigate the expression of key proteins and cellular processes involved in POM morphogenesis.
- To identify potential factors contributing to the abnormal ureter dilation in POM.
Main Methods:
- Analysis of ureter tissues from 14 pediatric patients with POM.
- Histological examination using hematoxylin and eosin staining.
- Immunohistochemistry for specific proteins (PGP 9.5, NGFR, TGFβ1, FGFR1, MMP-2, AT2R, SHH).
- Detection of apoptosis via terminal dUTP nick-end labeling (TUNL).
Main Results:
- POM tissues exhibited epithelial vacuolization, submucosal inflammation, and disorganized muscle layers.
- Increased apoptosis, MMP-2, FGFR1, and SHH expression were observed.
- Reduced TGFβ1 positive cell counts were noted in patients compared to controls.
- Correlations were found between MMP-2, FGFR1, and TGFβ1 expression in different ureter tissue layers.
Conclusions:
- POM pathogenesis involves epithelial and smooth muscle apoptosis, alongside tissue degradation.
- A disbalance in ureter wall remodeling, characterized by decreased TGFβ1 and increased FGFR1 and MMP-2, contributes to POM.
- These findings offer insights into the molecular mechanisms driving megaureter formation.
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