Ergosterol elicits oxidative burst in tobacco cells via phospholipase A2 and protein kinase C signal pathway.
Identifieur interne : 002333 ( Main/Exploration ); précédent : 002332; suivant : 002334Ergosterol elicits oxidative burst in tobacco cells via phospholipase A2 and protein kinase C signal pathway.
Auteurs : Tomas Kasparovsky [République tchèque] ; Jean-Pierre Blein ; Vladimir MikesSource :
- Plant physiology and biochemistry : PPB [ 0981-9428 ] ; 2004.
Descripteurs français
- KwdFr :
- Antienzymes (pharmacologie), Cellules cultivées (MeSH), Ergostérol (pharmacologie), Facteurs temps (MeSH), Isoquinoléines (pharmacologie), Néomycine (pharmacologie), Oestrènes (pharmacologie), Phospholipases A (antagonistes et inhibiteurs), Phospholipases A (métabolisme), Phospholipases A2 (MeSH), Protéine kinase C (métabolisme), Protéines d'algue (pharmacologie), Protéines fongiques (MeSH), Pyrrolidones (pharmacologie), Stress oxydatif (MeSH), Sulfonamides (MeSH), Survie cellulaire (MeSH), Tabac (effets des médicaments et des substances chimiques), Tabac (métabolisme), Transduction du signal (MeSH), Type C Phospholipases (antagonistes et inhibiteurs).
- MESH :
- antagonistes et inhibiteurs : Phospholipases A, Type C Phospholipases.
- effets des médicaments et des substances chimiques : Tabac.
- métabolisme : Phospholipases A, Protéine kinase C, Tabac.
- pharmacologie : Antienzymes, Ergostérol, Isoquinoléines, Néomycine, Oestrènes, Protéines d'algue, Pyrrolidones.
- Cellules cultivées, Facteurs temps, Phospholipases A2, Protéines fongiques, Stress oxydatif, Sulfonamides, Survie cellulaire, Transduction du signal.
English descriptors
- KwdEn :
- Algal Proteins (pharmacology), Cell Survival (MeSH), Cells, Cultured (MeSH), Enzyme Inhibitors (pharmacology), Ergosterol (pharmacology), Estrenes (pharmacology), Fungal Proteins (MeSH), Isoquinolines (pharmacology), Neomycin (pharmacology), Oxidative Stress (MeSH), Phospholipases A (antagonists & inhibitors), Phospholipases A (metabolism), Phospholipases A2 (MeSH), Protein Kinase C (metabolism), Pyrrolidinones (pharmacology), Signal Transduction (MeSH), Sulfonamides (MeSH), Time Factors (MeSH), Tobacco (drug effects), Tobacco (metabolism), Type C Phospholipases (antagonists & inhibitors).
- MESH :
- chemical , antagonists & inhibitors : Phospholipases A, Type C Phospholipases.
- chemical , metabolism : Phospholipases A, Protein Kinase C.
- chemical , pharmacology : Algal Proteins, Enzyme Inhibitors, Ergosterol, Estrenes, Isoquinolines, Neomycin, Pyrrolidinones.
- drug effects : Tobacco.
- metabolism : Tobacco.
- Cell Survival, Cells, Cultured, Fungal Proteins, Oxidative Stress, Phospholipases A2, Signal Transduction, Sulfonamides, Time Factors.
Abstract
Ergosterol, a typical fungal sterol, induced in tobacco (Nicotiana tabacum L. cv. Xanthi) suspension cells the synthesis of reactive oxygen species and alkalization of the external medium that are dependent on the mobilization of calcium from internal stores. We used specific inhibitors to elucidate the signal pathway triggered by ergosterol compared with cryptogein, a proteinaceous elicitor of Phytophthora cryptogea. Herbimycin A and genistein, inhibitors of tyrosine protein kinases, had no effect on the oxidative burst and pH changes induced by both elicitors. Similarly, H-89, an inhibitor of protein kinase A, had no effect on the induction of these defense reactions. However, the response to both elicitors was completely blocked by NPC-15437, a specific inhibitor of animal protein kinase C (PKC). The responses induced by cryptogein but not those induced by ergosterol were inhibited by U73122 and neomycin, inhibitors of phospholipase C (PLC). On the other hand, the activity of phospholipase A2 (PLA2) measured using a fluorogenic substrate was stimulated by ergosterol and not by cholesterol and cryptogein. A specific inhibitor of PLA2, arachidonic acid trifluoromethyl ketone (AACOCF3), inhibited the pathway stimulated by ergosterol but not that induced by cryptogein. These results suggest that the cryptogein-induced signal pathway leading to the oxidative burst and DeltapH changes includes PLC and PKC, whereas this response induced by ergosterol includes PLA2 and PKC.
DOI: 10.1016/j.plaphy.2004.04.003
PubMed: 15191747
Affiliations:
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xml:lang="en"><term>Algal Proteins (pharmacology)</term><term>Cell Survival (MeSH)</term><term>Cells, Cultured (MeSH)</term><term>Enzyme Inhibitors (pharmacology)</term><term>Ergosterol (pharmacology)</term><term>Estrenes (pharmacology)</term><term>Fungal Proteins (MeSH)</term><term>Isoquinolines (pharmacology)</term><term>Neomycin (pharmacology)</term><term>Oxidative Stress (MeSH)</term><term>Phospholipases A (antagonists & inhibitors)</term><term>Phospholipases A (metabolism)</term><term>Phospholipases A2 (MeSH)</term><term>Protein Kinase C (metabolism)</term><term>Pyrrolidinones (pharmacology)</term><term>Signal Transduction (MeSH)</term><term>Sulfonamides (MeSH)</term><term>Time Factors (MeSH)</term><term>Tobacco (drug effects)</term><term>Tobacco (metabolism)</term><term>Type C Phospholipases (antagonists & inhibitors)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Antienzymes (pharmacologie)</term><term>Cellules cultivées (MeSH)</term><term>Ergostérol (pharmacologie)</term><term>Facteurs temps (MeSH)</term><term>Isoquinoléines (pharmacologie)</term><term>Néomycine (pharmacologie)</term><term>Oestrènes (pharmacologie)</term><term>Phospholipases A (antagonistes et inhibiteurs)</term><term>Phospholipases A (métabolisme)</term><term>Phospholipases A2 (MeSH)</term><term>Protéine kinase C (métabolisme)</term><term>Protéines d'algue (pharmacologie)</term><term>Protéines fongiques (MeSH)</term><term>Pyrrolidones (pharmacologie)</term><term>Stress oxydatif (MeSH)</term><term>Sulfonamides (MeSH)</term><term>Survie cellulaire (MeSH)</term><term>Tabac (effets des médicaments et des substances chimiques)</term><term>Tabac (métabolisme)</term><term>Transduction du signal (MeSH)</term><term>Type C Phospholipases (antagonistes et inhibiteurs)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Phospholipases A</term><term>Type C Phospholipases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Phospholipases A</term><term>Protein Kinase C</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Algal Proteins</term><term>Enzyme Inhibitors</term><term>Ergosterol</term><term>Estrenes</term><term>Isoquinolines</term><term>Neomycin</term><term>Pyrrolidinones</term></keywords><keywords scheme="MESH" qualifier="antagonistes et inhibiteurs" xml:lang="fr"><term>Phospholipases A</term><term>Type C Phospholipases</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Phospholipases A</term><term>Protéine kinase C</term><term>Tabac</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Antienzymes</term><term>Ergostérol</term><term>Isoquinoléines</term><term>Néomycine</term><term>Oestrènes</term><term>Protéines d'algue</term><term>Pyrrolidones</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Survival</term><term>Cells, Cultured</term><term>Fungal Proteins</term><term>Oxidative Stress</term><term>Phospholipases A2</term><term>Signal Transduction</term><term>Sulfonamides</term><term>Time Factors</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Cellules cultivées</term><term>Facteurs temps</term><term>Phospholipases A2</term><term>Protéines fongiques</term><term>Stress oxydatif</term><term>Sulfonamides</term><term>Survie cellulaire</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Ergosterol, a typical fungal sterol, induced in tobacco (Nicotiana tabacum L. cv. Xanthi) suspension cells the synthesis of reactive oxygen species and alkalization of the external medium that are dependent on the mobilization of calcium from internal stores. We used specific inhibitors to elucidate the signal pathway triggered by ergosterol compared with cryptogein, a proteinaceous elicitor of Phytophthora cryptogea. Herbimycin A and genistein, inhibitors of tyrosine protein kinases, had no effect on the oxidative burst and pH changes induced by both elicitors. Similarly, H-89, an inhibitor of protein kinase A, had no effect on the induction of these defense reactions. However, the response to both elicitors was completely blocked by NPC-15437, a specific inhibitor of animal protein kinase C (PKC). The responses induced by cryptogein but not those induced by ergosterol were inhibited by U73122 and neomycin, inhibitors of phospholipase C (PLC). On the other hand, the activity of phospholipase A2 (PLA2) measured using a fluorogenic substrate was stimulated by ergosterol and not by cholesterol and cryptogein. A specific inhibitor of PLA2, arachidonic acid trifluoromethyl ketone (AACOCF3), inhibited the pathway stimulated by ergosterol but not that induced by cryptogein. These results suggest that the cryptogein-induced signal pathway leading to the oxidative burst and DeltapH changes includes PLC and PKC, whereas this response induced by ergosterol includes PLA2 and PKC.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">15191747</PMID><DateCompleted><Year>2004</Year><Month>08</Month><Day>26</Day></DateCompleted><DateRevised><Year>2020</Year><Month>09</Month><Day>30</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0981-9428</ISSN><JournalIssue CitedMedium="Print"><Volume>42</Volume><Issue>5</Issue><PubDate><Year>2004</Year><Month>May</Month></PubDate></JournalIssue><Title>Plant physiology and biochemistry : PPB</Title><ISOAbbreviation>Plant Physiol Biochem</ISOAbbreviation></Journal><ArticleTitle>Ergosterol elicits oxidative burst in tobacco cells via phospholipase A2 and protein kinase C signal pathway.</ArticleTitle><Pagination><MedlinePgn>429-35</MedlinePgn></Pagination><Abstract><AbstractText>Ergosterol, a typical fungal sterol, induced in tobacco (Nicotiana tabacum L. cv. Xanthi) suspension cells the synthesis of reactive oxygen species and alkalization of the external medium that are dependent on the mobilization of calcium from internal stores. We used specific inhibitors to elucidate the signal pathway triggered by ergosterol compared with cryptogein, a proteinaceous elicitor of Phytophthora cryptogea. Herbimycin A and genistein, inhibitors of tyrosine protein kinases, had no effect on the oxidative burst and pH changes induced by both elicitors. Similarly, H-89, an inhibitor of protein kinase A, had no effect on the induction of these defense reactions. However, the response to both elicitors was completely blocked by NPC-15437, a specific inhibitor of animal protein kinase C (PKC). The responses induced by cryptogein but not those induced by ergosterol were inhibited by U73122 and neomycin, inhibitors of phospholipase C (PLC). On the other hand, the activity of phospholipase A2 (PLA2) measured using a fluorogenic substrate was stimulated by ergosterol and not by cholesterol and cryptogein. A specific inhibitor of PLA2, arachidonic acid trifluoromethyl ketone (AACOCF3), inhibited the pathway stimulated by ergosterol but not that induced by cryptogein. These results suggest that the cryptogein-induced signal pathway leading to the oxidative burst and DeltapH changes includes PLC and PKC, whereas this response induced by ergosterol includes PLA2 and PKC.</AbstractText><CopyrightInformation>Copyright 2004 Elsevier SAS</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Kasparovsky</LastName><ForeName>Tomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Biochemistry, Masaryk University, Kotlarska 2, 61137 Brno, Czech Republic.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Blein</LastName><ForeName>Jean-Pierre</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Mikes</LastName><ForeName>Vladimir</ForeName><Initials>V</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>France</Country><MedlineTA>Plant Physiol Biochem</MedlineTA><NlmUniqueID>9882449</NlmUniqueID><ISSNLinking>0981-9428</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D020418">Algal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004791">Enzyme Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D004963">Estrenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005656">Fungal Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D007546">Isoquinolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011760">Pyrrolidinones</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013449">Sulfonamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C061032">cryptogein protein, Phytophthora cryptogea</NameOfSubstance></Chemical><Chemical><RegistryNumber>112648-68-7</RegistryNumber><NameOfSubstance UI="C060229">1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.7.11.13</RegistryNumber><NameOfSubstance UI="D011493">Protein Kinase C</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.32</RegistryNumber><NameOfSubstance UI="D010741">Phospholipases A</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.1.4</RegistryNumber><NameOfSubstance UI="D054467">Phospholipases A2</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 3.1.4.-</RegistryNumber><NameOfSubstance UI="D010738">Type C Phospholipases</NameOfSubstance></Chemical><Chemical><RegistryNumber>I16QD7X297</RegistryNumber><NameOfSubstance UI="D009355">Neomycin</NameOfSubstance></Chemical><Chemical><RegistryNumber>M876330O56</RegistryNumber><NameOfSubstance UI="C063509">N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide</NameOfSubstance></Chemical><Chemical><RegistryNumber>Z30RAY509F</RegistryNumber><NameOfSubstance UI="D004875">Ergosterol</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D020418" MajorTopicYN="N">Algal Proteins</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002470" MajorTopicYN="N">Cell Survival</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004791" MajorTopicYN="N">Enzyme Inhibitors</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004875" MajorTopicYN="N">Ergosterol</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004963" MajorTopicYN="N">Estrenes</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005656" MajorTopicYN="N">Fungal Proteins</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D007546" MajorTopicYN="N">Isoquinolines</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009355" MajorTopicYN="N">Neomycin</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="Y">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D010741" MajorTopicYN="N">Phospholipases A</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D054467" MajorTopicYN="N">Phospholipases A2</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D011493" MajorTopicYN="N">Protein Kinase C</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011760" MajorTopicYN="N">Pyrrolidinones</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D015398" MajorTopicYN="N">Signal Transduction</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013449" MajorTopicYN="Y">Sulfonamides</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013997" MajorTopicYN="N">Time Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014026" MajorTopicYN="N">Tobacco</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010738" MajorTopicYN="N">Type C Phospholipases</DescriptorName><QualifierName UI="Q000037" MajorTopicYN="N">antagonists & inhibitors</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2004</Year><Month>01</Month><Day>13</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2004</Year><Month>04</Month><Day>05</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2004</Year><Month>6</Month><Day>12</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2004</Year><Month>8</Month><Day>27</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2004</Year><Month>6</Month><Day>12</Day><Hour>5</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">15191747</ArticleId><ArticleId IdType="doi">10.1016/j.plaphy.2004.04.003</ArticleId><ArticleId IdType="pii">S0981-9428(04)00060-9</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République tchèque</li></country><region><li>Moravie</li></region><settlement><li>Brno</li></settlement></list><tree><noCountry><name sortKey="Blein, Jean Pierre" sort="Blein, Jean Pierre" uniqKey="Blein J" first="Jean-Pierre" last="Blein">Jean-Pierre Blein</name><name sortKey="Mikes, Vladimir" sort="Mikes, Vladimir" uniqKey="Mikes V" first="Vladimir" last="Mikes">Vladimir Mikes</name></noCountry><country name="République tchèque"><region name="Moravie"><name sortKey="Kasparovsky, Tomas" sort="Kasparovsky, Tomas" uniqKey="Kasparovsky T" first="Tomas" last="Kasparovsky">Tomas Kasparovsky</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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