How nerve growth factor drives physiological and inflammatory expressions of acid-sensing ion channel 3 in sensory neurons. Export

@article{citeulike:3758272, abstract = {Nerve growth factor (NGF) is a key element of inflammatory pain. It induces hyperalgesia by up-regulating 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 during 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 basal expression through constitutive activation of a trkA/phospholipase C/protein kinase C pathway, (ii). high inflammatory-like NGF induces ASIC3 overexpression through a trkA/JNK/p38MAPK pathway and a p75-dependent mechanism as a transcriptional switch, and (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.}, author = {Mamet, J. and Lazdunski, M. and Voilley, N.}, citeulike-article-id = {3758272}, citeulike-linkout-0 = {http://dx.doi.org/10.1074/jbc.M309468200}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/14522957}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=14522957}, doi = {10.1074/jbc.M309468200}, issn = {0021-9258}, journal = {The Journal of biological chemistry}, keywords = {asic3, neurons, ngf}, month = {December}, number = {49}, pages = {48907--48913}, posted-at = {2008-12-09 01:46:51}, priority = {3}, title = {How nerve growth factor drives physiological and inflammatory expressions of acid-sensing ion channel 3 in sensory neurons.}, url = {http://dx.doi.org/10.1074/jbc.M309468200}, volume = {278}, year = {2003} }

TY - JOUR ID - citeulike:3758272 L3 - citeulike-article-id:3758272 N2 - Nerve growth factor (NGF) is a key element of inflammatory pain. It induces hyperalgesia by up-regulating 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 during 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 basal expression through constitutive activation of a trkA/phospholipase C/protein kinase C pathway, (ii). high inflammatory-like NGF induces ASIC3 overexpression through a trkA/JNK/p38MAPK pathway and a p75-dependent mechanism as a transcriptional switch, and (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. IS - 49 JF - The Journal of biological chemistry SN - 0021-9258 EP - 48913 TI - How nerve growth factor drives physiological and inflammatory expressions of acid-sensing ion channel 3 in sensory neurons. VL - 278 SP - 48907 KW - asic3 KW - neurons KW - ngf AU - Mamet, J AU - Lazdunski, M AU - Voilley, N PY - 2003/12/05/ UR - http://dx.doi.org/10.1074/jbc.M309468200 ER -