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Papers In Press, published online ahead of print September 30, 2003
J. Biol. Chem, 10.1074/jbc.M309468200
Submitted on August 26, 2003
Revised on September 22, 2003
Accepted on September 29, 2003

How NGF drives physiological and inflammatory expressions of acid-sensing Ion channel 3 in sensory neurons

Julien Mamet, Michel Lazdunski, and Nicolas Voilley

Institut de Pharmacologie Moléculaire et Cellulaire, CNRS UMR6097, Valbonne 06560

Corresponding Author: voilley{at}ipmc.cnrs.fr

Nerve growth factor (NGF) is a key element of inflammatory pain. It induces hyperalgesia by upregulating the transcription of genes encoding receptors, ion channels and neuropeptides. Acid-sensing ion channel 3 (ASIC3), a depolarizing sodium channel gated by protons during tissue acidosis, is specifically expressed in sensory neurons. It has been associated to cardiac ischemic and inflammatory pains. We previously showed that low endogenous NGF was responsible for ASIC3 basal expression and high NGF durin g inflammation increased ASIC3 expression parallely to the development of neuron hyperexcitability associated with hyperalgesia. NGF is known to activate numerous signaling pathways through trkA and p75 receptors. We now show that (i) NGF controls ASIC3 b asal expression through constitutive activation of a trkA/PLC/PKC pathway, (ii) high inflammatory-like NGF induces ASIC3 overexpression through a trkA/JNK/p38MAPK pathway and a p75-dependent mechanism as a transcriptional switch, (iii) NGF acts through AP1 response elements in ASIC3 encoding gene promoter. These new data indicate potential targets that could be used to develop new treatments against inflammatory pain.


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