Up-regulation of NaV1.7 sodium channels expression by tumor necrosis factor-α in cultured bovine adrenal chromaffin cells and rat dorsal root ganglion neurons

Anesth Analg. 2014 Feb;118(2):318-324. doi: 10.1213/ANE.0000000000000085.

Abstract

Background: Tumor necrosis factor-α (TNF-α) is not only a key regulator of inflammatory response but also an important pain modulator. TNF-α enhances both tetrodotoxin-sensitive (TTX-S) and tetrodotoxin-resistant Na channel currents in dorsal root ganglion (DRG) neurons. However, it remains unknown whether TNF-α affects the function and expression of the TTX-S NaV1.7 Na channel, which plays crucial roles in pain generation.

Methods: We used cultured bovine adrenal chromaffin cells expressing the NaV1.7 Na channel isoform and compared them with cultured rat DRG neurons. The expression of TNF receptor 1 and 2 (TNFR1 and TNFR2) in adrenal chromaffin cells was studied by Semiquantitative reverse transcription-polymerase chain reaction. The effects of TNF-α on the expression of NaV1.7 were examined with reverse transcription-polymerase chain reaction and Western blot analysis. Results were expressed as mean ± SEM.

Results: TNFR1 and TNFR2 were expressed in adrenal chromaffin cells, as well as reported in DRG neurons. TNF-α up-regulated NaV1.7 mRNA by 132% ± 9% (N = 5, P = 0.004) in adrenal chromaffin cells, as well as 117% ± 2% (N = 5, P < 0.0001) in DRG neurons. Western blot analysis showed that TNF-α increased NaV1.7 protein up to 166% ± 24% (N = 5, corrected P < 0.0001) in adrenal chromaffin cells, concentration- and time-dependently.

Conclusions: TNF-α up-regulated NaV1.7 mRNA in both adrenal chromaffin cells and DRG neurons. In addition, TNF-α up-regulated the protein expression of the TTX-S NaV1.7 channel in adrenal chromaffin cells. Our findings may contribute to understanding the peripheral nociceptive mechanism of TNF-α.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Actins / metabolism
  • Adrenal Glands / metabolism*
  • Animals
  • Cattle
  • Chromaffin Cells / cytology*
  • Dose-Response Relationship, Drug
  • Female
  • Ganglia, Spinal / metabolism*
  • Male
  • NAV1.7 Voltage-Gated Sodium Channel / metabolism*
  • Neuralgia / drug therapy
  • Neurons / metabolism*
  • Rats
  • Receptors, Tumor Necrosis Factor, Type I / metabolism
  • Receptors, Tumor Necrosis Factor, Type II / metabolism
  • Reverse Transcriptase Polymerase Chain Reaction
  • Sodium / chemistry
  • Tetrodotoxin / chemistry
  • Time Factors
  • Tumor Necrosis Factor-alpha / metabolism*
  • Up-Regulation

Substances

  • Actins
  • NAV1.7 Voltage-Gated Sodium Channel
  • Receptors, Tumor Necrosis Factor, Type I
  • Receptors, Tumor Necrosis Factor, Type II
  • Scn9a protein, rat
  • Tnfrsf1a protein, rat
  • Tumor Necrosis Factor-alpha
  • Tetrodotoxin
  • Sodium