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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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STIM1 functionally couples to transient receptor potential ankyrin 1 contributing to nociception.

Yixiao Mei1,2, Hareram Birla1, Bo Hyun Lee2

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Summary

Stromal Interaction Molecule 1 (STIM1) is crucial for sensing cold, chemical, and mechanical pain stimuli. STIM1 deficiency in sensory neurons reduces pain responses, highlighting its role in nociception.

Keywords:
BradykininDorsal root ganglionEndoplasmic reticulumPainSTIM1Store-operated calcium channelsTRPA1

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pain Research

Background:

  • Stromal Interaction Molecule 1 (STIM1) is an endoplasmic reticulum (ER) calcium sensor.
  • STIM1 expression in nociceptors has been observed, but its functional role in pain sensing is unclear.
  • Transient Receptor Potential Ankyrin 1 (TRPA1) is a key sensor for noxious stimuli.

Purpose of the Study:

  • To investigate the functional significance of STIM1 in sensing various pain stimuli.
  • To elucidate the relationship between STIM1, TRPA1, and nociception.
  • To explore the downstream mechanisms of STIM1-mediated pain signaling.

Main Methods:

  • Utilized male and female mice models, including STIM1 conditional knockout and knockdown.
  • Performed immunostaining and Western blot to detect protein expression.
  • Measured calcium (Ca2+) entry and neuronal excitability in dorsal root ganglion neurons.
  • Administered TRPA1 agonists and ER Ca2+-ATPase inhibitors.

Main Results:

  • STIM1 deficiency significantly reduced responses to cold, chemical (TRPA1 agonist), and mechanical stimuli.
  • Activation of TRPA1 induced ER Ca2+ release, STIM1 translocation, and store-operated Ca2+ entry (SOCE).
  • STIM1-mediated SOCE enhanced neuronal excitability and reduced Kv4 potassium currents, a process dependent on the MAPK/ERK pathway.

Conclusions:

  • STIM1 acts as a critical transducer of nociceptive signals for diverse stimuli.
  • A novel link between STIM1 and TRPA1 in the ER was identified, contributing to TRPA1-mediated nociception.
  • STIM1 plays a significant role in regulating neuronal excitability and pain hypersensitivity.