Kir3.1 channel is functionally involved in TLR4-mediated signaling Academic Article uri icon

Overview

MeSH Major

  • Cytokines
  • G Protein-Coupled Inwardly-Rectifying Potassium Channels
  • Membrane Microdomains
  • Signal Transduction
  • Toll-Like Receptor 4

abstract

  • We aimed to study the involvement of Kir3.1 channel in TLR4-mediated signaling. LPS stimulation induced the recruitment of TLR4 and Kir3.1 into the lipid raft in THP-1 cells. Treatment with Tertiapin-Q, an inhibitor of Kir3.1, markedly abolished the recruitment of TLR4 into the lipid raft and inhibited the LPS-induced NF-κB activation, resulting in decreased production of TNF-α, IL-1β, and IL-6. To verify the specific role of the Kir3.1 channel, we generated Kir3.1-knockdown THP-1 cells. The Kir3.1(KD) THP-1 cells exhibited inhibition of NF-κB activation and production of these pro-inflammatory cytokines in response to TLR4 stimulation. Taken together, our results demonstrate that the Kir3.1 channel is involved in the TLR4-mediated signal at an early event by facilitating the recruitment of TLR4 into lipid raft.

publication date

  • April 22, 2011

Research

keywords

  • Academic Article

Identity

Language

  • eng

Digital Object Identifier (DOI)

  • 10.1016/j.bbrc.2011.03.076

PubMed ID

  • 21420934

Additional Document Info

start page

  • 687

end page

  • 91

volume

  • 407

number

  • 4