Related Experiment Video
Updated: Jun 15, 2026

Use of Ultra-high Field MRI in Small Rodent Models of Polycystic Kidney Disease for In Vivo Phenotyping and Drug Monitoring
Published on: June 23, 2015
Molecular events involved in the morphogenesis of multicystic dysplastic kidney
Salvatore Arena1, Carmine Fazzari, Maria Grazia Scuderi
1Unit of Pediatric Surgery, Department of Pediatric Surgery, University of Catania, Catania, Italy. arenasal @ inwind.it
Introduction:
Wnt-1 is capable of inducing metanephric mesenchyme to undergo tubulogenesis. A relationship between the degree of cystogenesis and reduced E-cadherin (E-cad) expression was described. Syndecan-1 (Sdc-1) has a critical role in kidney development.
Materials And Methods:
Ten multicystic dysplastic kidneys (MCDKs) were stained with hematoxylin and eosin and immunohistochemistry was performed using Wnt-1, E-cad and Sdc-1 antibodies. Eight unaffected kidneys were used as controls.
Results:
Strong Wnt-1 immunostaining occurred inside cystic/tubular epithelial cells and in blastematous foci. An immunoreaction was observed in glomerular epithelial cells. In controls, just weak cytoplasmic Wnt-1 positivity was seen in tubular epithelial cells. E-cad reaction was negative in MCDKs while strong immunostaining was common in tubular cells of controls. A strong Sdc-1 immunoreaction depicted cystic, tubular and glomerular epithelial cells in MCDKs while Sdc-1 expression documented weak positivity in tubular epithelium alone.
Conclusions:
Our data are in accordance with an involvement of Wnt-1 in normal nephrogenesis and with its role in altered epithelial differentiation of metanephric mesenchyme in MCDKs. Wnt-1 signal may function to suppress E-cad expression, a predisposing event for cystogenesis. High expression of Sdc-1 in tubular/cystic epithelial cells of MCDKs might alter the normal transition of stages of the developmental process and modify the anion charge of the glomerular barrier.
Insights
Wnt-1 signaling may drive cyst formation in multicystic dysplastic kidneys (MCDKs) by suppressing E-cadherin. Increased Syndecan-1 expression in MCDKs may also disrupt kidney development and glomerular function.
Area of Science:
- Nephrology
- Developmental Biology
- Molecular Biology
Background:
- Wnt-1 protein can induce tubulogenesis in metanephric mesenchyme.
- Reduced E-cadherin (E-cad) expression correlates with cystogenesis.
- Syndecan-1 (Sdc-1) plays a vital role in kidney development.
Purpose of the Study:
- To investigate the expression patterns of Wnt-1, E-cadherin, and Syndecan-1 in multicystic dysplastic kidneys (MCDKs).
- To elucidate the potential roles of these molecules in the pathogenesis of MCDKs.
Main Methods:
- Immunohistochemistry was used to analyze Wnt-1, E-cadherin, and Syndecan-1 expression in ten MCDKs and eight control kidneys.
- Hematoxylin and eosin staining was also performed.
Main Results:
- Strong Wnt-1 immunostaining was observed in cystic/tubular epithelial cells and blastematous foci in MCDKs, contrasting with weak positivity in control kidneys.
- E-cadherin expression was negative in MCDKs but strongly positive in control kidneys.
- Syndecan-1 showed strong immunoreaction in MCDK epithelial cells, whereas controls exhibited only weak positivity.
Conclusions:
- Wnt-1 is implicated in normal nephrogenesis and altered epithelial differentiation in MCDKs.
- Wnt-1 signaling may suppress E-cadherin, predisposing to cystogenesis.
- Elevated Syndecan-1 in MCDKs might disrupt kidney development and glomerular barrier function.
Related Concept Videos
Nephrons
Cleavage and Blastulation
