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Mechanically-gated ion channels are proteins found in eukaryotic and prokaryotic cell membranes that open in response to mechanical stress. Tension, compression, swelling, and shear stress can alter the conformation of the protein, opening a transmembrane channel that allows the passage of ions for signal transmission. In eukaryotes, mechanically-gated channels are distributed in several regions like the neurons, lungs, skin, bladder, and heart, where they play critical roles in numerous...
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Inflammatory signals enhance piezo2-mediated mechanosensitive currents.

Adrienne E Dubin1, Manuela Schmidt, Jayanti Mathur

  • 1Department of Cell Biology, The Scripps Research Institute, La Jolla, CA 92037, USA. adubin@scripps.edu

Cell Reports
|August 28, 2012
PubMed
Summary

Bradykinin (BK) enhances the activity of the piezo2 channel, a key player in mechanical pain sensation. This BK-induced sensitization of piezo2 may explain the development of mechanical hyperalgesia.

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Inflammatory mediators like bradykinin (BK) increase pain sensitivity (hyperalgesia).
  • While TRPV1 explains thermal hyperalgesia, the mechanisms of mechanical hyperalgesia remain unclear.
  • The role of the mechanically activated channel piezo2 in sensory neurons is unknown.

Purpose of the Study:

  • To investigate if bradykinin enhances piezo2 channel activity.
  • To determine the cellular mechanisms underlying BK-induced mechanical hyperalgesia.

Main Methods:

  • Utilized heterologous expression systems to study piezo2 channel function.
  • Examined the effects of bradykinin receptor beta 2 (BDKRB2) activation on piezo2.
  • Investigated the involvement of protein kinase A (PKA) and protein kinase C (PKC) signaling pathways.
  • Measured piezo2-dependent currents in native sensory neurons.

Main Results:

  • Bradykinin significantly increased piezo2 current amplitude and slowed its inactivation.
  • PKA and PKC agonists enhanced piezo2 activity.
  • BDKRB2-mediated potentiation of piezo2 was blocked by PKA and PKC inhibitors.
  • BK enhanced native piezo2-dependent currents eightfold via PKA and PKC.

Conclusions:

  • Bradykinin enhances piezo2 channel activity through BDKRB2, PKA, and PKC.
  • Piezo2 sensitization is a potential cellular mechanism contributing to bradykinin-induced mechanical hyperalgesia.