Role of autophagy in nerve cell apoptosis in mice infected with street rabies virus.
Identifieur interne : 000053 ( Main/Exploration ); précédent : 000052; suivant : 000054Role of autophagy in nerve cell apoptosis in mice infected with street rabies virus.
Auteurs : Fatemeh Hosseini Heydarabadi [Iran] ; Asghar Abdoli [Iran] ; Safoora Gharibzadeh [Iran] ; Mohammad Sayyah [Iran] ; Rouzbeh Bashar [Iran] ; Farzaneh Sheikholeslami [Iran]Source :
- Archives of virology [ 1432-8798 ] ; 2020.
Descripteurs français
- KwdFr :
- Adénine (analogues et dérivés), Adénine (pharmacologie), Animaux (MeSH), Apoptose (MeSH), Autophagie (MeSH), Encéphale (anatomopathologie), Encéphale (virologie), Modèles animaux de maladie humaine (MeSH), Neurones (cytologie), Neurones (virologie), Protéines virales (métabolisme), Rage (maladie) (anatomopathologie), Rage (maladie) (virologie), Réplication virale (MeSH), Sirolimus (pharmacologie), Souris (MeSH), Technique d'immunofluorescence directe (MeSH), Virus de la rage (génétique), Virus de la rage (physiologie).
- MESH :
- analogues et dérivés : Adénine.
- anatomopathologie : Encéphale, Rage (maladie).
- cytologie : Neurones.
- génétique : Virus de la rage.
- métabolisme : Protéines virales.
- pharmacologie : Adénine, Sirolimus.
- physiologie : Virus de la rage.
- virologie : Encéphale, Neurones, Rage (maladie).
- Animaux, Apoptose, Autophagie, Modèles animaux de maladie humaine, Réplication virale, Souris, Technique d'immunofluorescence directe.
English descriptors
- KwdEn :
- Adenine (analogs & derivatives), Adenine (pharmacology), Animals (MeSH), Apoptosis (MeSH), Autophagy (MeSH), Brain (pathology), Brain (virology), Disease Models, Animal (MeSH), Fluorescent Antibody Technique, Direct (MeSH), Mice (MeSH), Neurons (cytology), Neurons (virology), Rabies (pathology), Rabies (virology), Rabies virus (genetics), Rabies virus (physiology), Sirolimus (pharmacology), Viral Proteins (metabolism), Virus Replication (MeSH).
- MESH :
- chemical , analogs & derivatives : Adenine.
- chemical , metabolism : Viral Proteins.
- chemical , pharmacology : Adenine, Sirolimus.
- cytology : Neurons.
- genetics : Rabies virus.
- pathology : Brain, Rabies.
- physiology : Rabies virus.
- virology : Brain, Neurons, Rabies.
- Animals, Apoptosis, Autophagy, Disease Models, Animal, Fluorescent Antibody Technique, Direct, Mice, Virus Replication.
Abstract
Rabies is an important zoonotic disease in Iran. Autophagy is a process that maintains homeostasis and can be used as an innate defense mechanism against viruses. Apoptosis is the process of programmed cell death induced by physiological and pathological conditions. The crosstalk of autophagy and apoptosis plays a key role in rabies virus infection. In the current study, NMRI mice intra-cranially received 3-Methyl Adenine (3-MA), rapamycin, street rabies virus (SRABV) and drugs plus SRABV. SRABV and Map1lc3, Beclin-1, Atg5 gene expression were assayed by real-time PCR. Immunohistochemistry was carried out via LC3 protein staining as an autophagy marker, and apoptotic cell death was measured using a TUNEL assay. Map1lc3, Beclin-1 and Atg5 genes expression was significantly increased in drug-plus-SRBV-treated tissues compared to control at 24 hpi. Map1lc3 and Atg5 gene expression showed a slight change in the drugs-plus-virus group compared with the control at 72 hpi. The presence of LC3 in the tissues of the group treated with rapamycin plus SRBV confirmed induction of autophagy, but it was not present in the tissues treated with 3-MA plus SRBV. Our data revealed that apoptosis was induced only in the groups receiving the SRBV or rapamycin or both at 24 hpi. Apoptosis was observed after 72 hours, when the drugs' effect had disappeared in all but the autophagy inhibitor group. Understanding the interaction of SRABV with autophagy pathway genes and its effect on host cell apoptosis may open a new horizon for human intervention and allow a deeper understanding of rabies infections.
DOI: 10.1007/s00705-020-04815-z
PubMed: 33034763
Affiliations:
Links toward previous steps (curation, corpus...)
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Pasteur Institute of Iran, No. 75-12 Farvardin Street, 1316943551, Tehran</wicri:regionArea><wicri:noRegion>Tehran</wicri:noRegion></affiliation></author></analytic><series><title level="j">Archives of virology</title><idno type="eISSN">1432-8798</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adenine (analogs & derivatives)</term><term>Adenine (pharmacology)</term><term>Animals (MeSH)</term><term>Apoptosis (MeSH)</term><term>Autophagy (MeSH)</term><term>Brain (pathology)</term><term>Brain (virology)</term><term>Disease Models, Animal (MeSH)</term><term>Fluorescent Antibody Technique, Direct (MeSH)</term><term>Mice (MeSH)</term><term>Neurons (cytology)</term><term>Neurons (virology)</term><term>Rabies (pathology)</term><term>Rabies (virology)</term><term>Rabies virus (genetics)</term><term>Rabies virus (physiology)</term><term>Sirolimus (pharmacology)</term><term>Viral Proteins (metabolism)</term><term>Virus Replication (MeSH)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Adénine (analogues et dérivés)</term><term>Adénine (pharmacologie)</term><term>Animaux (MeSH)</term><term>Apoptose (MeSH)</term><term>Autophagie (MeSH)</term><term>Encéphale (anatomopathologie)</term><term>Encéphale (virologie)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Neurones (cytologie)</term><term>Neurones (virologie)</term><term>Protéines virales (métabolisme)</term><term>Rage (maladie) (anatomopathologie)</term><term>Rage (maladie) (virologie)</term><term>Réplication virale (MeSH)</term><term>Sirolimus (pharmacologie)</term><term>Souris (MeSH)</term><term>Technique d'immunofluorescence directe (MeSH)</term><term>Virus de la rage (génétique)</term><term>Virus de la rage (physiologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Adenine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Viral Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Adenine</term><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="analogues et dérivés" xml:lang="fr"><term>Adénine</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Encéphale</term><term>Rage (maladie)</term></keywords><keywords scheme="MESH" qualifier="cytologie" xml:lang="fr"><term>Neurones</term></keywords><keywords scheme="MESH" qualifier="cytology" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Rabies virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Virus de la rage</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Protéines virales</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Rabies</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Adénine</term><term>Sirolimus</term></keywords><keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Virus de la rage</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Rabies virus</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Encéphale</term><term>Neurones</term><term>Rage (maladie)</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Brain</term><term>Neurons</term><term>Rabies</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Disease Models, Animal</term><term>Fluorescent Antibody Technique, Direct</term><term>Mice</term><term>Virus Replication</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Apoptose</term><term>Autophagie</term><term>Modèles animaux de maladie humaine</term><term>Réplication virale</term><term>Souris</term><term>Technique d'immunofluorescence directe</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Rabies is an important zoonotic disease in Iran. Autophagy is a process that maintains homeostasis and can be used as an innate defense mechanism against viruses. Apoptosis is the process of programmed cell death induced by physiological and pathological conditions. The crosstalk of autophagy and apoptosis plays a key role in rabies virus infection. In the current study, NMRI mice intra-cranially received 3-Methyl Adenine (3-MA), rapamycin, street rabies virus (SRABV) and drugs plus SRABV. SRABV and Map1lc3, Beclin-1, Atg5 gene expression were assayed by real-time PCR. Immunohistochemistry was carried out via LC3 protein staining as an autophagy marker, and apoptotic cell death was measured using a TUNEL assay. Map1lc3, Beclin-1 and Atg5 genes expression was significantly increased in drug-plus-SRBV-treated tissues compared to control at 24 hpi. Map1lc3 and Atg5 gene expression showed a slight change in the drugs-plus-virus group compared with the control at 72 hpi. The presence of LC3 in the tissues of the group treated with rapamycin plus SRBV confirmed induction of autophagy, but it was not present in the tissues treated with 3-MA plus SRBV. Our data revealed that apoptosis was induced only in the groups receiving the SRBV or rapamycin or both at 24 hpi. Apoptosis was observed after 72 hours, when the drugs' effect had disappeared in all but the autophagy inhibitor group. Understanding the interaction of SRABV with autophagy pathway genes and its effect on host cell apoptosis may open a new horizon for human intervention and allow a deeper understanding of rabies infections.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">33034763</PMID><DateCompleted><Year>2020</Year><Month>11</Month><Day>05</Day></DateCompleted><DateRevised><Year>2020</Year><Month>11</Month><Day>05</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1432-8798</ISSN><JournalIssue CitedMedium="Internet"><Volume>165</Volume><Issue>12</Issue><PubDate><Year>2020</Year><Month>Dec</Month></PubDate></JournalIssue><Title>Archives of virology</Title><ISOAbbreviation>Arch Virol</ISOAbbreviation></Journal><ArticleTitle>Role of autophagy in nerve cell apoptosis in mice infected with street rabies virus.</ArticleTitle><Pagination><MedlinePgn>2857-2867</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1007/s00705-020-04815-z</ELocationID><Abstract><AbstractText>Rabies is an important zoonotic disease in Iran. Autophagy is a process that maintains homeostasis and can be used as an innate defense mechanism against viruses. Apoptosis is the process of programmed cell death induced by physiological and pathological conditions. The crosstalk of autophagy and apoptosis plays a key role in rabies virus infection. In the current study, NMRI mice intra-cranially received 3-Methyl Adenine (3-MA), rapamycin, street rabies virus (SRABV) and drugs plus SRABV. SRABV and Map1lc3, Beclin-1, Atg5 gene expression were assayed by real-time PCR. Immunohistochemistry was carried out via LC3 protein staining as an autophagy marker, and apoptotic cell death was measured using a TUNEL assay. Map1lc3, Beclin-1 and Atg5 genes expression was significantly increased in drug-plus-SRBV-treated tissues compared to control at 24 hpi. Map1lc3 and Atg5 gene expression showed a slight change in the drugs-plus-virus group compared with the control at 72 hpi. The presence of LC3 in the tissues of the group treated with rapamycin plus SRBV confirmed induction of autophagy, but it was not present in the tissues treated with 3-MA plus SRBV. Our data revealed that apoptosis was induced only in the groups receiving the SRBV or rapamycin or both at 24 hpi. Apoptosis was observed after 72 hours, when the drugs' effect had disappeared in all but the autophagy inhibitor group. Understanding the interaction of SRABV with autophagy pathway genes and its effect on host cell apoptosis may open a new horizon for human intervention and allow a deeper understanding of rabies infections.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Heydarabadi</LastName><ForeName>Fatemeh Hosseini</ForeName><Initials>FH</Initials><AffiliationInfo><Affiliation>Department of Rabies, Pasteur Institute of Iran, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Abdoli</LastName><ForeName>Asghar</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Department of Hepatitis and AIDS, Pasteur Institute of Iran, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gharibzadeh</LastName><ForeName>Safoora</ForeName><Initials>S</Initials><AffiliationInfo><Affiliation>Department of Epidemiology and Biostatistics, Research Centre for Emerging and Reemerging Infectious Diseases, Pasteur Institute of Iran, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sayyah</LastName><ForeName>Mohammad</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bashar</LastName><ForeName>Rouzbeh</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Rabies, Pasteur Institute of Iran, Tehran, Iran.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sheikholeslami</LastName><ForeName>Farzaneh</ForeName><Initials>F</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-2835-548X</Identifier><AffiliationInfo><Affiliation>Department of Rabies, Pasteur Institute of Iran, Tehran, Iran. f_sheikh@psateur.ac.ir.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Rabies Laboratory, Virology Department, Pasteur Institute of Iran, No. 75-12 Farvardin Street, 1316943551, Tehran, Iran. f_sheikh@psateur.ac.ir.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>564</GrantID><Agency>Pasteur Institute of Iran</Agency><Country></Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>10</Month><Day>09</Day></ArticleDate></Article><MedlineJournalInfo><Country>Austria</Country><MedlineTA>Arch Virol</MedlineTA><NlmUniqueID>7506870</NlmUniqueID><ISSNLinking>0304-8608</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014764">Viral Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>5142-23-4</RegistryNumber><NameOfSubstance UI="C025946">3-methyladenine</NameOfSubstance></Chemical><Chemical><RegistryNumber>JAC85A2161</RegistryNumber><NameOfSubstance UI="D000225">Adenine</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000225" MajorTopicYN="N">Adenine</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D017209" MajorTopicYN="Y">Apoptosis</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001343" MajorTopicYN="Y">Autophagy</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="Y">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D019085" MajorTopicYN="N">Fluorescent Antibody Technique, Direct</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009474" MajorTopicYN="N">Neurons</DescriptorName><QualifierName UI="Q000166" MajorTopicYN="Y">cytology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011818" MajorTopicYN="N">Rabies</DescriptorName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="N">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011820" MajorTopicYN="N">Rabies virus</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000502" MajorTopicYN="Y">physiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014764" MajorTopicYN="N">Viral Proteins</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D014779" MajorTopicYN="N">Virus Replication</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>07</Month><Day>15</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>08</Month><Day>17</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>10</Month><Day>10</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>11</Month><Day>6</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>10</Month><Day>9</Day><Hour>12</Hour><Minute>11</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">33034763</ArticleId><ArticleId IdType="doi">10.1007/s00705-020-04815-z</ArticleId><ArticleId IdType="pii">10.1007/s00705-020-04815-z</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Iran</li></country></list><tree><country name="Iran"><noRegion><name sortKey="Heydarabadi, Fatemeh Hosseini" sort="Heydarabadi, Fatemeh Hosseini" uniqKey="Heydarabadi F" first="Fatemeh Hosseini" last="Heydarabadi">Fatemeh Hosseini Heydarabadi</name></noRegion><name sortKey="Abdoli, Asghar" sort="Abdoli, Asghar" uniqKey="Abdoli A" first="Asghar" last="Abdoli">Asghar Abdoli</name><name sortKey="Bashar, Rouzbeh" sort="Bashar, Rouzbeh" uniqKey="Bashar R" first="Rouzbeh" last="Bashar">Rouzbeh Bashar</name><name sortKey="Gharibzadeh, Safoora" sort="Gharibzadeh, Safoora" uniqKey="Gharibzadeh S" first="Safoora" last="Gharibzadeh">Safoora Gharibzadeh</name><name sortKey="Sayyah, Mohammad" sort="Sayyah, Mohammad" uniqKey="Sayyah M" first="Mohammad" last="Sayyah">Mohammad Sayyah</name><name sortKey="Sheikholeslami, Farzaneh" sort="Sheikholeslami, Farzaneh" uniqKey="Sheikholeslami F" first="Farzaneh" last="Sheikholeslami">Farzaneh Sheikholeslami</name><name sortKey="Sheikholeslami, Farzaneh" sort="Sheikholeslami, Farzaneh" uniqKey="Sheikholeslami F" first="Farzaneh" last="Sheikholeslami">Farzaneh Sheikholeslami</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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