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Aldosterone regulates microRNAs in the cortical collecting duct to alter sodium transport

Robert S Edinger1, Claudia Coronnello2, Andrew J Bodnar3

  • 1Renal-Electrolyte Division.

Journal of the American Society of Nephrology : JASN
|April 19, 2014
PubMed

Insights

MicroRNAs (miRs) are newly found to regulate kidney sodium transport. Aldosterone alters miR expression, impacting epithelial sodium channel (ENaC) activity and ankyrin 3 protein levels in kidney cells.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Genetics

Background:

  • The role of microRNAs (miRs) in kidney sodium transport regulation is not well understood.
  • Aldosterone is a key hormone regulating sodium balance in the kidney.

Purpose of the Study:

  • To investigate the role of aldosterone in regulating miR expression in kidney cells.
  • To determine the impact of aldosterone-regulated miRs on sodium transport and identify their targets.

Main Methods:

  • Microarray analysis to identify aldosterone-regulated miRs in mouse cortical collecting duct (mCCD) cells.
  • Quantitative RT-PCR to confirm miR expression changes.
  • Functional assays to assess the effect of miRs on epithelial sodium channel (ENaC)-mediated sodium transport.
  • Computational prediction (ComiR) and experimental validation of miR targets, including ankyrin 3 (Ank3).

Main Results:

  • Aldosterone significantly altered miR expression in mCCD cells and primary distal nephron principal cells.
  • Downregulation of specific miRs (mmu-miR-335-3p, mmu-miR-290-5p, mmu-miR-1983) increased ENaC-mediated sodium transport.
  • Overexpression of these miRs blunted aldosterone's effect on ENaC transport.
  • Ankyrin 3 (Ank3) was identified as a direct target of these miRs and influenced ENaC activity.

Conclusions:

  • MicroRNAs act as intermediaries in aldosterone signaling within kidney principal cells.
  • Aldosterone-regulated miRs modulate sodium transport by targeting proteins like ankyrin 3.
  • This study establishes a novel mechanism for physiological regulation of sodium homeostasis in the kidney.

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