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TNF inhibits AQP2 expression via a miR137-dependent pathway.

Shoujin Hao1, AnnMarie DelliPizzi2, Anna Pia Lasaracina1

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American Journal of Physiology. Renal Physiology
|November 16, 2023
PubMed
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Tumor necrosis factor (TNF) regulates kidney aquaporin-2 (AQP2) expression through miR-137. This pathway impacts kidney function and electrolyte balance, revealing a novel mechanism for blood pressure regulation.

Keywords:
aquaporin-2cytokinesdietary saltmiR-137tumor necrosis factor-α

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Area of Science:

  • Renal physiology
  • Molecular biology
  • Immunology

Background:

  • Tumor necrosis factor (TNF) is known to inhibit extrarenal aquaporin (AQP) expression.
  • MicroRNA-137 (miR-137) is a regulator of aquaporin-2 (AQP2) expression.
  • The interaction between TNF, miR-137, and AQP2 in the kidney remains unclear.

Purpose of the Study:

  • To investigate if TNF inhibits renal AQP2 expression via a miR-137-dependent mechanism.
  • To elucidate the role of TNF and miR-137 in regulating kidney water and electrolyte balance.

Main Methods:

  • Primary renal inner medullary collecting duct (IMCD) cells were used for in vitro experiments.
  • Techniques included miRNA mimic transfection, TNF silencing via lentivirus, and exposure to hypertonic medium.
  • In vivo studies involved intrarenal lentivirus silencing of TNF in mice and measurement of urine parameters.

Main Results:

  • miR-137 directly targets and decreases AQP2 mRNA and protein expression in IMCD cells.
  • Hypertonic conditions increased both miR-137 and TNF expression in IMCD cells.
  • TNF upregulates miR-137 expression, and silencing TNF increased AQP2 levels and affected kidney diluting ability.

Conclusions:

  • TNF inhibits renal AQP2 expression through a miR-137-dependent mechanism.
  • This pathway plays a role in regulating kidney function, electrolyte balance, and potentially blood pressure.
  • Cytokines like TNF are emerging as key mediators in physiological responses beyond inflammation.