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Aldosterone induces ras methylation in A6 epithelia

N F Al-Baldawi1, J D Stockand, O K Al-Khalili

  • 1Center for Cell and Molecular Signaling, Department of Physiology, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

American Journal of Physiology. Cell Physiology
|July 27, 2000
PubMed

Insights

Aldosterone enhances sodium reabsorption through protein methylation, particularly targeting Ras proteins. Inhibiting Ras methylation or expression blocks this crucial sodium channel activity.

Area of Science:

  • Renal Physiology
  • Molecular Endocrinology
  • Cellular Biology

Background:

  • Aldosterone is a key hormone regulating sodium reabsorption in the kidneys.
  • Acute effects of aldosterone (<4 hours) are linked to protein methylation.
  • Understanding the molecular mechanisms of aldosterone action is crucial for renal physiology.

Purpose of the Study:

  • To investigate the relationship between protein methylation and aldosterone's action.
  • To identify aldosterone-mediated targets for protein methylation in cultured renal cells.
  • To elucidate the role of protein methylation in aldosterone-induced sodium transport.

Main Methods:

  • Measurement of protein methylation levels and methyltransferase activity in cultured renal cells (A6).
  • Utilizing methyltransferase inhibitors, including a specific inhibitor for isoprenyl-cysteine methyltransferase (S-trans, trans-farnesylthiosalicylic acid).
  • Analysis of aldosterone-induced protein methylation at specific molecular weights and assessment of Ras protein and its methylation.
  • Investigating the effect of Ras antisense oligonucleotides on Na(+) channel activity.

Main Results:

  • Aldosterone significantly increased protein methylation and methyltransferase activity.
  • A specific methyltransferase inhibitor completely blocked aldosterone-induced protein methylation and short-circuit current.
  • Aldosterone induced protein methylation near 90 kDa and 20 kDa, with the latter corresponding to small G proteins like Ras.
  • Aldosterone increased Ras protein levels and methylation, and Ras inhibition reduced Na(+) channel activity.

Conclusions:

  • Protein methylation is essential for aldosterone-induced increases in sodium transport.
  • p21(Ras) is identified as a key target for aldosterone-mediated protein methylation.
  • Inhibition of Ras expression or methylation significantly impairs Na(+) channel activity, highlighting its role in aldosterone signaling.

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