Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/9434
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dc.contributor.authorLallemend, F-
dc.contributor.authorLefebvre, PP-
dc.contributor.authorHans, G-
dc.contributor.authorRIGO, Jean-Michel-
dc.contributor.authorVan De Water, TR-
dc.contributor.authorMoonen, G-
dc.contributor.authorMalgrange, B.-
dc.date.accessioned2009-04-08T12:53:59Z-
dc.date.issued2003-
dc.identifier.citationJOURNAL OF NEUROCHEMISTRY, 87(2). p. 508-521-
dc.identifier.issn0022-3042-
dc.identifier.urihttp://hdl.handle.net/1942/9434-
dc.description.abstractIn the current study, we have investigated the ability of substance P (SP) to protect 3-day-old (P3) rat spiral ganglion neurons (SGNs) from trophic factor deprivation (TFD)-induced cell death. The presence of SP high affinity neurokinin-1 receptor (NK1) transcripts was detected in the spiral ganglion and the NK1 protein localized to SGNs both ex vivo and in vitro. Treatment with SP increased cytoplasmic Ca2+ in SGNs, further arguing for the presence of functional NK1 on these neurons. Both SP and the agonist [Sar(9), Met(O-2)(11)]-SP significantly decreased SGN cell death induced by TFD, with no effect on neurite outgrowth. The survival promoting effect of SP was blocked by the NK1 antagonist, WIN51708. Both pan-caspase inhibitor BOC-D-FMK and SP treatments markedly reduced activation of caspases and DNA fragmentation in trophic factor deprived-neurons. The neuroprotective action of SP was antagonised by specific inhibitors of second messengers, including 1.2-bis-(O-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid (BAPTA-AM) to chelate cytosolic Ca2+, the protein kinase C (PKC) inhibitors bisindolylmaleimide I, Go6976 and LY333531 and the MAPK/ERK inhibitor U0126. In contrast, nifedipine, a specific inhibitor of L-type Ca2+ channel, and LY294002, a phosphatidylinositol-3-OH kinase (PI3K) inhibitor, had no effect on SP trophic support of SGNs. Moreover, activation of endogenous PKC by 4beta-phorbol 12-myristate 13-acetate (PMA) also reduced the loss of trophic factor-deprived SGNs. Thus, NK1 expressed by SGNs transmit a survival-promoting regulatory signal during TFD-induced SGN cell death via pathways involving PKC activation, Ca2+ signalling and MAPK/ERK activation, which can be accounted for by an inhibition of caspase activation.-
dc.language.isoen-
dc.publisherBLACKWELL PUBLISHING LTD-
dc.subject.otherapoptosis; neuroprotection; NK1; spiral ganglion neurons; substance P-
dc.titleSubstance P protects spiral ganglion neurons from apoptosis via PKC-Ca2+-MAPK/ERK pathways-
dc.typeJournal Contribution-
dc.identifier.epage521-
dc.identifier.issue2-
dc.identifier.spage508-
dc.identifier.volume87-
local.bibliographicCitation.jcatA1-
dc.description.notesUniv Liege, Res Ctr Cellular & Mol Neurobiol, Liege, Belgium. Univ Liege, Dept Otorhinolaryngol, Liege, Belgium. Univ Liege, Dept Neurol, Liege, Belgium. Univ Miami, Sch Med, Dept Otolaryngol, Miami, FL USA.-
local.type.refereedRefereed-
local.type.specifiedReview-
dc.bibliographicCitation.oldjcatA1-
dc.identifier.doi10.1046/j.1471-4159.2003.02014.x-
dc.identifier.isi000185596100024-
item.fulltextNo Fulltext-
item.accessRightsClosed Access-
item.contributorVan De Water, TR-
item.contributorMoonen, G-
item.contributorLefebvre, PP-
item.contributorHans, G-
item.contributorMalgrange, B.-
item.contributorLallemend, F-
item.contributorRIGO, Jean-Michel-
item.fullcitationLallemend, F; Lefebvre, PP; Hans, G; RIGO, Jean-Michel; Van De Water, TR; Moonen, G & Malgrange, B. (2003) Substance P protects spiral ganglion neurons from apoptosis via PKC-Ca2+-MAPK/ERK pathways. In: JOURNAL OF NEUROCHEMISTRY, 87(2). p. 508-521.-
crisitem.journal.issn0022-3042-
crisitem.journal.eissn1471-4159-
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