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Updated: Feb 22, 2026

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Published on: December 31, 2013
CXCL1 activates TRPV1 via Gi/o protein and actin filaments
Alexandru Florian Deftu1, Alexandru Filippi2, Roxana Olimpia Gheorghe1
1Department of Anatomy, Animal Physiology and Biophysics, Faculty of Biology, University of Bucharest, Splaiul Independenţei 91-95, 050095 Bucharest, Romania.
Aims:
CXCL1 is a chemokine with pleiotropic effects, including pain and itch. Itch, an unpleasant sensation that elicits the desire or reflex to scratch, it is evoked mainly from the skin and implicates activation of a specific subset of IB4+, C-type primary afferents. In previous studies we showed that acute application of CXCL1 induced a Ca2+ influx of low amplitude and slow kinetics in a subpopulation of transient receptor potential vanilloid type 1 (TRPV1)+/isolectin B4 (IB4)+dorsal root ganglia neurons which also responded to other itch-inducing agents. In this study we explored the mechanism behind the Ca2+ influx to better understand how CXCL1 acts on primary sensitive neurons to induce itch.
Materials And Methods:
Intracellular Ca2+ imaging and patch-clamp recordings on dorsal root ganglia neurons primary cultures and HEK293T cell transiently transfected with TRPV1 and CXCR2 plasmids were used to investigate the acute effect (12min application) of 4nM CXCL1. In primary cultures, the focus was on TRPV1+/IB4+ cells to which the itch-sensitive neurons belong.
Key Findings:
The results showed that the Ca2+ influx induced by the acute application of CXCL1 is mediated mainly by TRPV1 receptors and depends on extracellular Ca2+ not on intracellular stores. TRPV1 was activated, not sensitized by CXCL1, in a CXCR2 receptors- and actin filaments-dependent manner, since specific blockers and actin depolymerizing agents disrupted the CXCL1 effect.
Significance:
This study brings additional data about the itch inducing mechanism of CXCL1 chemokine and about a new mechanism of TRPV1 activation via actin filaments.
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