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MiR193a Modulation and Podocyte Phenotype.

Alok Jha1, Shourav Saha1, Kamesh Ayasolla1

  • 1Institute of Molecular Medicine, Feinstein Institute for Medical Research and Zucker School of Medicine at Hofstra-North well, New York, NY 11030, USA.

Cells
|April 23, 2020
PubMed
Summary
This summary is machine-generated.

The Apolipoprotein L1 (APOL1)-miR193a axis regulates podocyte homeostasis. Down-regulating miR193a enhances APOL1 and podocyte differentiation markers, suggesting a therapeutic strategy.

Keywords:
APOL1RXRSox2VDRWT1YY1miR193a

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • The Apolipoprotein L1 (APOL1)-miR193a axis is crucial for podocyte homeostasis.
  • Transcription factors like YY1, WT1, Sox2, and VDR-RXR heterodimer potentially regulate miR193a expression.
  • Understanding this axis is key to podocyte health and disease.

Purpose of the Study:

  • To investigate the regulatory roles of transcription factors on miR193a expression in human podocytes.
  • To elucidate the impact of the miR193a-APOL1 interaction on podocyte molecular phenotype.
  • To explore the therapeutic potential of modulating miR193a for podocyte differentiation.

Main Methods:

  • Computational modeling and docking to predict transcription factor binding to the miR193a promoter.
  • Molecular Dynamic (MD) simulations to analyze interactions between miR193a, transcription factors, and APOL1 3' UTR.
  • In vitro experiments involving inhibition and overexpression of miR193a and silencing of transcription factors in undifferentiated and differentiated podocytes.

Main Results:

  • MD simulations confirmed interactions between miR193a and YY1, WT1, Sox2, VDR, and APOL1 3' UTR.
  • Undifferentiated podocytes showed high miR193a, YY1, Sox2, and low WT1, VDR, APOL1; differentiated podocytes showed the inverse.
  • miR193a inhibition in undifferentiated podocytes increased APOL1 and differentiation markers; conversely, miR193a overexpression in differentiated podocytes decreased them.
  • Silencing YY1/Sox2 in undifferentiated podocytes decreased miR193a and increased VDR/CD2AP.
  • Silencing WT1/VDR in differentiated podocytes increased miR193a, YY1, and Sox2.

Conclusions:

  • miR193a plays a critical role in regulating podocyte differentiation and APOL1 expression.
  • The interplay between miR193a, transcription factors (YY1, WT1, Sox2, VDR), and APOL1 is central to podocyte phenotype.
  • Down-regulation of miR193a, potentially via VDR agonists, represents a promising therapeutic strategy to enhance podocyte differentiation markers.