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        <identifier>oai:hiroshima.repo.nii.ac.jp:02006384</identifier>
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        <jpcoar:jpcoar xmlns:datacite="https://schema.datacite.org/meta/kernel-4/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:dcndl="http://ndl.go.jp/dcndl/terms/" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:jpcoar="https://github.com/JPCOAR/schema/blob/master/2.0/" xmlns:oaire="http://namespace.openaire.eu/schema/oaire/" xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:rioxxterms="http://www.rioxx.net/schema/v2.0/rioxxterms/" xmlns:xs="http://www.w3.org/2001/XMLSchema" xmlns="https://github.com/JPCOAR/schema/blob/master/2.0/" xsi:schemaLocation="https://github.com/JPCOAR/schema/blob/master/2.0/jpcoar_scm.xsd">
          <dc:title xml:lang="en">Interleukin-1 inhibits voltage-dependent P/Q-type Ca2+ channel associated with the inhibition of the rise of intracellular free Ca2+ concentration and catecholamine release in adrenal chromaffin cells</dc:title>
          <jpcoar:creator>
            <jpcoar:creatorName xml:lang="en">Morita, Katsuya</jpcoar:creatorName>
            <jpcoar:familyName xml:lang="en">Morita</jpcoar:familyName>
            <jpcoar:givenName xml:lang="en">Katsuya</jpcoar:givenName>
          </jpcoar:creator>
          <jpcoar:creator>
            <jpcoar:creatorName xml:lang="en">Miyasako, Takanori</jpcoar:creatorName>
            <jpcoar:familyName xml:lang="en">Miyasako</jpcoar:familyName>
            <jpcoar:givenName xml:lang="en">Takanori</jpcoar:givenName>
          </jpcoar:creator>
          <jpcoar:creator>
            <jpcoar:creatorName xml:lang="en">Kitayama, Shigeo</jpcoar:creatorName>
            <jpcoar:familyName xml:lang="en">Kitayama</jpcoar:familyName>
            <jpcoar:givenName xml:lang="en">Shigeo</jpcoar:givenName>
          </jpcoar:creator>
          <jpcoar:creator>
            <jpcoar:creatorName xml:lang="en">Dohi, Toshihiro</jpcoar:creatorName>
            <jpcoar:familyName xml:lang="en">Dohi</jpcoar:familyName>
            <jpcoar:givenName xml:lang="en">Toshihiro</jpcoar:givenName>
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          <dc:rights>Copyright (c) 2004 Elsevier B.V</dc:rights>
          <jpcoar:subject subjectScheme="Other">IL-1</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">Voltage-dependent Ca2+ channel</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">P/Q-type Ca2+ channel</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">Catecholamine release</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">Ca2+</jpcoar:subject>
          <jpcoar:subject subjectScheme="Other">Adrenal chromaffin cells</jpcoar:subject>
          <jpcoar:subject subjectScheme="NDC">490</jpcoar:subject>
          <datacite:description xml:lang="en">Effects of interleukin (IL) on intracellular free Ca2+ concentration ([Ca2+]i) rise and catecholamine (CA) release were examined in isolated, cultured bovine adrenal chromaffin cells. IL-1α and IL-1β inhibited the rise of [Ca2+]i and CA release induced by acetylcholine (ACh) and excess KCl both in normal and in Ca2+-sucrose medium. IL-1 receptor antagonist, IL-1RA by pretreatment blocked the inhibitory actions of IL-1. IL-1α reduced CA release induced by veratridine in normal medium but not in the presence of diltiazem. Analysis using specific blockers for voltage-operated Ca2+ channels revealed that IL-1α specifically inhibited the P/Q-type Ca2+ channel to reduce [Ca2+]i rise induced by excess KCl. IL-1 did not affect [Ca2+]i rise induced either by bradykinin or caffeine in Ca2+- deprivated medium or via activation of store-operated Ca2+ channel. The inhibitory effects of IL-1 were blocked by pretreatments of cells with herbimycin A, U0126 and PD 98054, but not with SB202190, SP 600125 or pertussis toxin (PTX), inhibited the induction of the inhibitory action of IL-1.These results demonstrated that IL-1 inhibits stimulation-evoked [Ca2+]i rise and CA release in chromaffin cells by blocking voltage-operated P/O-type Ca2+ channels. The inhibitory action of IL-1 may be mediated through tyrosine kinase and MEK/ERK pathways.</datacite:description>
          <dc:publisher>Elsevier B.V</dc:publisher>
          <datacite:date dateType="Issued">2004-08-04</datacite:date>
          <dc:language>eng</dc:language>
          <dc:type rdf:resource="http://purl.org/coar/resource_type/c_6501">journal article</dc:type>
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          <jpcoar:identifier identifierType="URI">https://hiroshima.repo.nii.ac.jp/records/2006384</jpcoar:identifier>
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            <jpcoar:relatedIdentifier identifierType="DOI">10.1016/j.bbagen.2004.04.012</jpcoar:relatedIdentifier>
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            <jpcoar:relatedIdentifier identifierType="DOI">http://dx.doi.org/10.1016/j.bbagen.2004.04.012</jpcoar:relatedIdentifier>
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          <jpcoar:sourceIdentifier identifierType="ISSN">0304-4165</jpcoar:sourceIdentifier>
          <jpcoar:sourceIdentifier identifierType="NCID">AA00564679</jpcoar:sourceIdentifier>
          <jpcoar:sourceTitle>Biochimica et Biophysica Acta</jpcoar:sourceTitle>
          <jpcoar:sourceTitle>Biochimica et Biophysica Acta</jpcoar:sourceTitle>
          <jpcoar:volume>1673</jpcoar:volume>
          <jpcoar:issue>3</jpcoar:issue>
          <jpcoar:pageStart>160</jpcoar:pageStart>
          <jpcoar:pageStart>160</jpcoar:pageStart>
          <jpcoar:pageEnd>169</jpcoar:pageEnd>
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