PUBLICATION

Role of Monovalent Ions in the NKCC1 Inhibition Mechanism Revealed through Molecular Simulations

Authors
Janoš, P., Magistrato, A.
ID
ZDB-PUB-221212-11
Date
2022
Source
International Journal of Molecular Sciences   23(23): (Journal)
Registered Authors
Keywords
drug design, dynamic docking, enhanced sampling, ion transporters, membrane transporters, molecular dynamics, monovalent ions
MeSH Terms
  • Chlorides/metabolism
  • Sodium/metabolism
  • Bumetanide*/pharmacology
  • Humans
  • Animals
  • Solute Carrier Family 12, Member 2
  • Potassium/metabolism
  • Zebrafish*/metabolism
PubMed
36499764 Full text @ Int. J. Mol. Sci.
Abstract
The secondary active Na-K-Cl cotransporter 1 (NKCC1) promotes electroneutral uptake of two chloride ions, one sodium ion and one potassium ion. NKCC1 regulates Cl- homeostasis, thus being implicated in transepithelial water transport and in neuronal excitability. Aberrant NKCC1 transport is linked to a variety of human diseases. The loop diuretic drugs bumetanide, furosemide, azosemide and ethacrynic acid target NKCC1, but are characterized by poor selectivity leading to severe side effects. Despite its therapeutic importance, the molecular details of the NKCC1 inhibition mechanism remain unclear. Using all-atom simulations, we predict a putative binding mode of these drugs to the zebrafish (z) and human (h) NKCC1 orthologs. Although differing in their specific interactions with NKCC1 and/or monovalent ions, all drugs can fit within the same cavity and engage in hydrophobic interactions with M304/M382 in z/hNKCC1, a proposed ion gating residue demonstrated to be key for bumetanide binding. Consistent with experimental evidence, all drugs take advantage of the K+/Na+ ions, which plastically respond to their binding. This study not only provides atomic-level insights useful for drug discovery campaigns of more selective/potent NKCC1 inhibitors aimed to tackle diseases related to deregulated Cl- homeostasis, but it also supplies a paradigmatic example of the key importance of dynamical effects when drug binding is mediated by monovalent ions.
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