"Autophagic flux" in normal mouse tissues: focus on endogenous LC3A processing.
Identifieur interne : 000372 ( PubMed/Corpus ); précédent : 000371; suivant : 000373"Autophagic flux" in normal mouse tissues: focus on endogenous LC3A processing.
Auteurs : Christos E. Zois ; Alexandra Giatromanolaki ; Efthimios Sivridis ; Marina Papaiakovou ; Heikki Kainulainen ; Michael I. KoukourakisSource :
- Autophagy [ 1554-8635 ] ; 2011.
English descriptors
- KwdEn :
- Adaptor Proteins, Signal Transducing (metabolism), Animals, Antibody Specificity (immunology), Apoptosis Regulatory Proteins (metabolism), Autophagy (drug effects), Autophagy (radiation effects), Beclin-1, Chloroquine (pharmacology), Gene Expression Regulation (drug effects), Gene Expression Regulation (radiation effects), Heat-Shock Proteins (metabolism), Hepatocytes (cytology), Hepatocytes (drug effects), Hepatocytes (metabolism), Hepatocytes (radiation effects), Humans, Immunohistochemistry, Liver (cytology), Liver (drug effects), Liver (metabolism), Male, Mice, Mice, Inbred BALB C, Microtubule-Associated Proteins (genetics), Microtubule-Associated Proteins (immunology), Microtubule-Associated Proteins (metabolism), Organ Specificity (drug effects), Organ Specificity (radiation effects), Protein Processing, Post-Translational (drug effects), Protein Processing, Post-Translational (radiation effects), RNA, Messenger (genetics), RNA, Messenger (metabolism), Radiation, Ionizing, Sequestosome-1 Protein.
- MESH :
- chemical , genetics : Microtubule-Associated Proteins, RNA, Messenger.
- chemical , immunology : Microtubule-Associated Proteins.
- chemical , metabolism : Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins, Heat-Shock Proteins, Microtubule-Associated Proteins, RNA, Messenger.
- cytology : Hepatocytes, Liver.
- drug effects : Autophagy, Gene Expression Regulation, Hepatocytes, Liver, Organ Specificity, Protein Processing, Post-Translational.
- immunology : Antibody Specificity.
- metabolism : Hepatocytes, Liver.
- chemical , pharmacology : Chloroquine.
- radiation effects : Autophagy, Gene Expression Regulation, Hepatocytes, Organ Specificity, Protein Processing, Post-Translational.
- Animals, Beclin-1, Humans, Immunohistochemistry, Male, Mice, Mice, Inbred BALB C, Radiation, Ionizing, Sequestosome-1 Protein.
Abstract
Autophagy is a major intracellular pathway for the degradation and recycling of long-lived proteins, mature ribosomes and even entire organelles. The best studied autophagic marker is the LC3B and it is believed that only the amount of the LC3B-II correlates with the amount of the autophagic membranes. Whether the LC3A processing, aside to LC3B, is a valuable endogenous 'autophagic flux' marker is far less clear. The specificity of rabbit polyclonal antibodies to the LC3A and the LC3B was tested against the commercial available human recombinant proteins LC3A and LC3B. In order to measure 'autophagic flux' in mouse liver, lung, kidney and heart we used: (1) a lysosomotropic reagent chloroquine, which inhibit the intra-lysosomal acidification or their fusion with autophagosome, (2) nutrient starvation as an autophagic stimulus and (3) ionizing radiation, which is known to destabilize lysosomes. According to the immunoblotting work the LC3A protein follows discrete patterns of LC3A-I and LC3A-II changes in liver, lung, kidney and heart tissues of mice, whereas the LC3B protein didn't follow the same pattern under stressor conditions. We conclude that the endogenous LC3A processing is a major marker of autophagy flux in mouse model. Fractionated samples (soluble vs. membrane fractions) should be used in immunoblotting to allow discrimination between the LC3-I soluble and the LC3-II membrane protein and kinetics. Further, when dealing with in vivo models it is necessary to check the specificity of the antibodies used against the LC3A and LC3B proteins as their expression and responsiveness is not overlapping.
DOI: 10.4161/auto.7.11.16664
PubMed: 21997374
Links to Exploration step
pubmed:21997374Le document en format XML
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Zois</name><affiliation><nlm:affiliation>Department of Radiotherapy-Oncology, Democritus University of Thrace Medical School, University General Hospital of Alexandroupolis, Alexandroupolis, Greece.</nlm:affiliation></affiliation></author><author><name sortKey="Giatromanolaki, Alexandra" sort="Giatromanolaki, Alexandra" uniqKey="Giatromanolaki A" first="Alexandra" last="Giatromanolaki">Alexandra Giatromanolaki</name></author><author><name sortKey="Sivridis, Efthimios" sort="Sivridis, Efthimios" uniqKey="Sivridis E" first="Efthimios" last="Sivridis">Efthimios Sivridis</name></author><author><name sortKey="Papaiakovou, Marina" sort="Papaiakovou, Marina" uniqKey="Papaiakovou M" first="Marina" last="Papaiakovou">Marina Papaiakovou</name></author><author><name sortKey="Kainulainen, Heikki" sort="Kainulainen, Heikki" uniqKey="Kainulainen H" first="Heikki" last="Kainulainen">Heikki Kainulainen</name></author><author><name sortKey="Koukourakis, Michael I" sort="Koukourakis, Michael I" uniqKey="Koukourakis M" first="Michael I" last="Koukourakis">Michael I. Koukourakis</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21997374</idno><idno type="pmid">21997374</idno><idno type="doi">10.4161/auto.7.11.16664</idno><idno type="wicri:Area/PubMed/Corpus">000372</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000372</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">"Autophagic flux" in normal mouse tissues: focus on endogenous LC3A processing.</title><author><name sortKey="Zois, Christos E" sort="Zois, Christos E" uniqKey="Zois C" first="Christos E" last="Zois">Christos E. Zois</name><affiliation><nlm:affiliation>Department of Radiotherapy-Oncology, Democritus University of Thrace Medical School, University General Hospital of Alexandroupolis, Alexandroupolis, Greece.</nlm:affiliation></affiliation></author><author><name sortKey="Giatromanolaki, Alexandra" sort="Giatromanolaki, Alexandra" uniqKey="Giatromanolaki A" first="Alexandra" last="Giatromanolaki">Alexandra Giatromanolaki</name></author><author><name sortKey="Sivridis, Efthimios" sort="Sivridis, Efthimios" uniqKey="Sivridis E" first="Efthimios" last="Sivridis">Efthimios Sivridis</name></author><author><name sortKey="Papaiakovou, Marina" sort="Papaiakovou, Marina" uniqKey="Papaiakovou M" first="Marina" last="Papaiakovou">Marina Papaiakovou</name></author><author><name sortKey="Kainulainen, Heikki" sort="Kainulainen, Heikki" uniqKey="Kainulainen H" first="Heikki" last="Kainulainen">Heikki Kainulainen</name></author><author><name sortKey="Koukourakis, Michael I" sort="Koukourakis, Michael I" uniqKey="Koukourakis M" first="Michael I" last="Koukourakis">Michael I. Koukourakis</name></author></analytic><series><title level="j">Autophagy</title><idno type="eISSN">1554-8635</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptor Proteins, Signal Transducing (metabolism)</term><term>Animals</term><term>Antibody Specificity (immunology)</term><term>Apoptosis Regulatory Proteins (metabolism)</term><term>Autophagy (drug effects)</term><term>Autophagy (radiation effects)</term><term>Beclin-1</term><term>Chloroquine (pharmacology)</term><term>Gene Expression Regulation (drug effects)</term><term>Gene Expression Regulation (radiation effects)</term><term>Heat-Shock Proteins (metabolism)</term><term>Hepatocytes (cytology)</term><term>Hepatocytes (drug effects)</term><term>Hepatocytes (metabolism)</term><term>Hepatocytes (radiation effects)</term><term>Humans</term><term>Immunohistochemistry</term><term>Liver (cytology)</term><term>Liver (drug effects)</term><term>Liver (metabolism)</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Microtubule-Associated Proteins (genetics)</term><term>Microtubule-Associated Proteins (immunology)</term><term>Microtubule-Associated Proteins (metabolism)</term><term>Organ Specificity (drug effects)</term><term>Organ Specificity (radiation effects)</term><term>Protein Processing, Post-Translational (drug effects)</term><term>Protein Processing, Post-Translational (radiation effects)</term><term>RNA, Messenger (genetics)</term><term>RNA, Messenger (metabolism)</term><term>Radiation, Ionizing</term><term>Sequestosome-1 Protein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Microtubule-Associated Proteins</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Microtubule-Associated Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Adaptor Proteins, Signal Transducing</term><term>Apoptosis Regulatory Proteins</term><term>Heat-Shock Proteins</term><term>Microtubule-Associated Proteins</term><term>RNA, Messenger</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Hepatocytes</term><term>Liver</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Autophagy</term><term>Gene Expression Regulation</term><term>Hepatocytes</term><term>Liver</term><term>Organ Specificity</term><term>Protein Processing, Post-Translational</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antibody Specificity</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Hepatocytes</term><term>Liver</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Chloroquine</term></keywords><keywords scheme="MESH" qualifier="radiation effects" xml:lang="en"><term>Autophagy</term><term>Gene Expression Regulation</term><term>Hepatocytes</term><term>Organ Specificity</term><term>Protein Processing, Post-Translational</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Beclin-1</term><term>Humans</term><term>Immunohistochemistry</term><term>Male</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Radiation, Ionizing</term><term>Sequestosome-1 Protein</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Autophagy is a major intracellular pathway for the degradation and recycling of long-lived proteins, mature ribosomes and even entire organelles. The best studied autophagic marker is the LC3B and it is believed that only the amount of the LC3B-II correlates with the amount of the autophagic membranes. Whether the LC3A processing, aside to LC3B, is a valuable endogenous 'autophagic flux' marker is far less clear. The specificity of rabbit polyclonal antibodies to the LC3A and the LC3B was tested against the commercial available human recombinant proteins LC3A and LC3B. In order to measure 'autophagic flux' in mouse liver, lung, kidney and heart we used: (1) a lysosomotropic reagent chloroquine, which inhibit the intra-lysosomal acidification or their fusion with autophagosome, (2) nutrient starvation as an autophagic stimulus and (3) ionizing radiation, which is known to destabilize lysosomes. According to the immunoblotting work the LC3A protein follows discrete patterns of LC3A-I and LC3A-II changes in liver, lung, kidney and heart tissues of mice, whereas the LC3B protein didn't follow the same pattern under stressor conditions. We conclude that the endogenous LC3A processing is a major marker of autophagy flux in mouse model. Fractionated samples (soluble vs. membrane fractions) should be used in immunoblotting to allow discrimination between the LC3-I soluble and the LC3-II membrane protein and kinetics. Further, when dealing with in vivo models it is necessary to check the specificity of the antibodies used against the LC3A and LC3B proteins as their expression and responsiveness is not overlapping.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">21997374</PMID><DateCompleted><Year>2012</Year><Month>02</Month><Day>22</Day></DateCompleted><DateRevised><Year>2016</Year><Month>11</Month><Day>25</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1554-8635</ISSN><JournalIssue CitedMedium="Internet"><Volume>7</Volume><Issue>11</Issue><PubDate><Year>2011</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Autophagy</Title><ISOAbbreviation>Autophagy</ISOAbbreviation></Journal><ArticleTitle>"Autophagic flux" in normal mouse tissues: focus on endogenous LC3A processing.</ArticleTitle><Pagination><MedlinePgn>1371-8</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.4161/auto.7.11.16664</ELocationID><Abstract><AbstractText>Autophagy is a major intracellular pathway for the degradation and recycling of long-lived proteins, mature ribosomes and even entire organelles. The best studied autophagic marker is the LC3B and it is believed that only the amount of the LC3B-II correlates with the amount of the autophagic membranes. Whether the LC3A processing, aside to LC3B, is a valuable endogenous 'autophagic flux' marker is far less clear. The specificity of rabbit polyclonal antibodies to the LC3A and the LC3B was tested against the commercial available human recombinant proteins LC3A and LC3B. In order to measure 'autophagic flux' in mouse liver, lung, kidney and heart we used: (1) a lysosomotropic reagent chloroquine, which inhibit the intra-lysosomal acidification or their fusion with autophagosome, (2) nutrient starvation as an autophagic stimulus and (3) ionizing radiation, which is known to destabilize lysosomes. According to the immunoblotting work the LC3A protein follows discrete patterns of LC3A-I and LC3A-II changes in liver, lung, kidney and heart tissues of mice, whereas the LC3B protein didn't follow the same pattern under stressor conditions. We conclude that the endogenous LC3A processing is a major marker of autophagy flux in mouse model. Fractionated samples (soluble vs. membrane fractions) should be used in immunoblotting to allow discrimination between the LC3-I soluble and the LC3-II membrane protein and kinetics. Further, when dealing with in vivo models it is necessary to check the specificity of the antibodies used against the LC3A and LC3B proteins as their expression and responsiveness is not overlapping.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Zois</LastName><ForeName>Christos E</ForeName><Initials>CE</Initials><AffiliationInfo><Affiliation>Department of Radiotherapy-Oncology, Democritus University of Thrace Medical School, University General Hospital of Alexandroupolis, Alexandroupolis, Greece.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Giatromanolaki</LastName><ForeName>Alexandra</ForeName><Initials>A</Initials></Author><Author ValidYN="Y"><LastName>Sivridis</LastName><ForeName>Efthimios</ForeName><Initials>E</Initials></Author><Author ValidYN="Y"><LastName>Papaiakovou</LastName><ForeName>Marina</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Kainulainen</LastName><ForeName>Heikki</ForeName><Initials>H</Initials></Author><Author ValidYN="Y"><LastName>Koukourakis</LastName><ForeName>Michael I</ForeName><Initials>MI</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><ArticleDate DateType="Electronic"><Year>2011</Year><Month>11</Month><Day>01</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Autophagy</MedlineTA><NlmUniqueID>101265188</NlmUniqueID><ISSNLinking>1554-8627</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D048868">Adaptor Proteins, Signal Transducing</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D051017">Apoptosis Regulatory 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mouse</NameOfSubstance></Chemical><Chemical><RegistryNumber>886U3H6UFF</RegistryNumber><NameOfSubstance UI="D002738">Chloroquine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D048868" MajorTopicYN="N">Adaptor Proteins, Signal Transducing</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000918" MajorTopicYN="N">Antibody Specificity</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051017" MajorTopicYN="N">Apoptosis Regulatory Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000071186" MajorTopicYN="N">Beclin-1</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002738" MajorTopicYN="N">Chloroquine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005786" MajorTopicYN="N">Gene Expression Regulation</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006360" MajorTopicYN="N">Heat-Shock Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D022781" MajorTopicYN="N">Hepatocytes</DescriptorName><QualifierName UI="Q000166" 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MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008807" MajorTopicYN="N">Mice, Inbred BALB C</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008869" MajorTopicYN="N">Microtubule-Associated Proteins</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D009928" MajorTopicYN="Y">Organ Specificity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011499" MajorTopicYN="Y">Protein Processing, Post-Translational</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName><QualifierName UI="Q000528" MajorTopicYN="N">radiation effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012333" MajorTopicYN="N">RNA, Messenger</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011839" MajorTopicYN="N">Radiation, Ionizing</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000071456" MajorTopicYN="N">Sequestosome-1 Protein</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>10</Month><Day>15</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate 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