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Data supporting the regulation of FOXC2 in podocyte dysfunction.
Neeta Datta1, Sonja Lindfors1, Naoyuki Miura2
1Department of Pathology, University of Helsinki, 00290 Helsinki, Finland.
Data in Brief
|February 24, 2016
Summary
This study examines podocyte injury markers in obese rats and the role of FOXC2 in human podocytes. Findings reveal FOXC2
Area of Science:
- Nephrology
- Molecular Biology
- Cell Biology
Background:
- Podocyte injury is a key factor in kidney disease progression.
- Obesity and diabetes are associated with increased risk of kidney damage.
- The transcription factor FOXC2 is implicated in cellular processes relevant to podocyte function.
Purpose of the Study:
- To investigate podocyte injury markers in obese Zucker rat glomeruli.
- To determine the effect of FOXC2 overexpression on actin dynamics and ZO-1 expression in human podocytes.
- To analyze the impact of obesity and diabetes-associated factors on FOXC2 expression in podocytes.
Main Methods:
- Analysis of podocyte injury markers and nephrin expression in rat glomeruli.
- Overexpression of FOXC2 in differentiated human podocytes to assess F-/G-actin ratio and ZO-1 levels.
- Treatment of differentiated podocytes with obesity/diabetes-related factors to evaluate FOXC2 expression changes.
Main Results:
- Expression levels of specific podocyte injury markers and nephrin were measured in obese versus lean Zucker rat glomeruli.
- FOXC2 overexpression altered the F-/G-actin ratio and ZO-1 expression in cultured human podocytes.
- Treatments mimicking obesity and diabetes conditions affected FOXC2 expression in differentiated podocytes.
Conclusions:
- The data provide insights into podocyte injury mechanisms potentially mediated by FOXC2.
- FOXC2 may play a role in regulating cytoskeletal dynamics and cell-cell junctions in podocytes.
- These findings contribute to understanding the link between metabolic diseases and podocyte dysfunction.
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