RapamycinFungusV1, Main, Exploration, bibRecord, 000386

Autophagy Promotes Porcine Parvovirus Replication and Induces Non-Apoptotic Cell Death in Porcine Placental Trophoblasts.

Identifieur interne : 000386 ( Main/Exploration ); précédent : 000385; suivant : 000387

Autophagy Promotes Porcine Parvovirus Replication and Induces Non-Apoptotic Cell Death in Porcine Placental Trophoblasts.

Auteurs : Xiujuan Zhang ; Yingli Xiong ; Jie Zhang [République populaire de Chine] ; Ting Shao [République populaire de Chine] ; Songbiao Chen [République populaire de Chine] ; Bichen Miao [République populaire de Chine] ; Zhenyu Wang [République populaire de Chine] ; Qian Du [République populaire de Chine] ; Yong Huang [République populaire de Chine] ; Dewen Tong [République populaire de Chine]

Source :

Viruses [ 1999-4915 ] ; 2019.

RBID : pubmed:31861933

Descripteurs français

KwdFr :
- Animaux (MeSH), Apoptose (MeSH), Autophagie (MeSH), Autophagosomes (métabolisme), Femelle (MeSH), Grossesse (MeSH), Infections à Parvoviridae (médecine vétérinaire), Lignée cellulaire (MeSH), Lysosomes (métabolisme), Maladies des porcs (métabolisme), Maladies des porcs (virologie), Marqueurs biologiques (MeSH), Parvovirus porcin (physiologie), Parvovirus porcin (ultrastructure), Placenta (métabolisme), Placenta (virologie), Réplication virale (MeSH), Suidae (MeSH), Trophoblastes (métabolisme), Trophoblastes (virologie).
MESH :
- médecine vétérinaire : Infections à Parvoviridae.
- métabolisme : Autophagosomes, Lysosomes, Maladies des porcs, Placenta, Trophoblastes.
- physiologie : Parvovirus porcin.
- virologie : Maladies des porcs, Placenta, Trophoblastes.
- Animaux, Apoptose, Autophagie, Femelle, Grossesse, Lignée cellulaire, Marqueurs biologiques, Parvovirus porcin, Réplication virale, Suidae.

English descriptors

KwdEn :
- Animals (MeSH), Apoptosis (MeSH), Autophagosomes (metabolism), Autophagy (MeSH), Biomarkers (MeSH), Cell Line (MeSH), Female (MeSH), Lysosomes (metabolism), Parvoviridae Infections (veterinary), Parvovirus, Porcine (physiology), Parvovirus, Porcine (ultrastructure), Placenta (metabolism), Placenta (virology), Pregnancy (MeSH), Swine (MeSH), Swine Diseases (metabolism), Swine Diseases (virology), Trophoblasts (metabolism), Trophoblasts (virology), Virus Replication (MeSH).
MESH :
- chemical : Biomarkers.
- metabolism : Autophagosomes, Lysosomes, Placenta, Swine Diseases, Trophoblasts.
- physiology : Parvovirus, Porcine.
- ultrastructure : Parvovirus, Porcine.
- veterinary : Parvoviridae Infections.
- virology : Placenta, Swine Diseases, Trophoblasts.
- Animals, Apoptosis, Autophagy, Cell Line, Female, Pregnancy, Swine, Virus Replication.

Abstract

Autophagy plays important roles in the infection and pathogenesis of many viruses, yet the regulatory roles of autophagy in the process of porcine parvovirus (PPV) infection remain unclear. Herein, we show that PPV infection induces autophagy in porcine placental trophoblasts (PTCs). Induction of autophagy by rapamycin (RAPA) inhibited the occurrence of apoptotic cell death, yet promoted viral replication in PPV-infected cells; inhibition of autophagy by 3-MA or ATG5 knockdown increased cellular apoptosis and reduced PPV replication. Interestingly, we found that in the presence of caspase-inhibitor zVAD-fmk, PPV induces non-apoptotic cell death that was characterized by lysosomal damage and associated with autophagy. Induction of complete autophagy flux by RAPA markedly promoted PPV replication compared with incomplete autophagy induced by RAPA plus bafilomycin (RAPA/BAF) in the early phase of PPV infection (24 h.p.i.). Meanwhile, induction of complete autophagy with RAPA increased lysosomal damage and non-apoptotic cell death in the later phase of PPV infection. Therefore, our data suggest that autophagy can enhance PPV replication and promote the occurrence of lysosomal-damage-associated non-apoptotic cell death in PPV-infected porcine placental trophoblasts.

DOI: 10.3390/v12010015
PubMed: 31861933
PubMed Central: PMC7020067

Affiliations:

République populaire de Chine

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000143
to stream Main, to step Curation: 000143

Le document en format XML

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<term>Apoptosis (MeSH)</term>
<term>Autophagosomes (metabolism)</term>
<term>Autophagy (MeSH)</term>
<term>Biomarkers (MeSH)</term>
<term>Cell Line (MeSH)</term>
<term>Female (MeSH)</term>
<term>Lysosomes (metabolism)</term>
<term>Parvoviridae Infections (veterinary)</term>
<term>Parvovirus, Porcine (physiology)</term>
<term>Parvovirus, Porcine (ultrastructure)</term>
<term>Placenta (metabolism)</term>
<term>Placenta (virology)</term>
<term>Pregnancy (MeSH)</term>
<term>Swine (MeSH)</term>
<term>Swine Diseases (metabolism)</term>
<term>Swine Diseases (virology)</term>
<term>Trophoblasts (metabolism)</term>
<term>Trophoblasts (virology)</term>
<term>Virus Replication (MeSH)</term>
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<keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term>
<term>Apoptose (MeSH)</term>
<term>Autophagie (MeSH)</term>
<term>Autophagosomes (métabolisme)</term>
<term>Femelle (MeSH)</term>
<term>Grossesse (MeSH)</term>
<term>Infections à Parvoviridae (médecine vétérinaire)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Lysosomes (métabolisme)</term>
<term>Maladies des porcs (métabolisme)</term>
<term>Maladies des porcs (virologie)</term>
<term>Marqueurs biologiques (MeSH)</term>
<term>Parvovirus porcin (physiologie)</term>
<term>Parvovirus porcin (ultrastructure)</term>
<term>Placenta (métabolisme)</term>
<term>Placenta (virologie)</term>
<term>Réplication virale (MeSH)</term>
<term>Suidae (MeSH)</term>
<term>Trophoblastes (métabolisme)</term>
<term>Trophoblastes (virologie)</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Biomarkers</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Autophagosomes</term>
<term>Lysosomes</term>
<term>Placenta</term>
<term>Swine Diseases</term>
<term>Trophoblasts</term>
</keywords>
<keywords scheme="MESH" qualifier="médecine vétérinaire" xml:lang="fr"><term>Infections à Parvoviridae</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Autophagosomes</term>
<term>Lysosomes</term>
<term>Maladies des porcs</term>
<term>Placenta</term>
<term>Trophoblastes</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Parvovirus porcin</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Parvovirus, Porcine</term>
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<keywords scheme="MESH" qualifier="ultrastructure" xml:lang="en"><term>Parvovirus, Porcine</term>
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<term>Trophoblastes</term>
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<term>Trophoblasts</term>
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<term>Autophagy</term>
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<term>Autophagie</term>
<term>Femelle</term>
<term>Grossesse</term>
<term>Lignée cellulaire</term>
<term>Marqueurs biologiques</term>
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<front><div type="abstract" xml:lang="en">Autophagy plays important roles in the infection and pathogenesis of many viruses, yet the regulatory roles of autophagy in the process of porcine parvovirus (PPV) infection remain unclear. Herein, we show that PPV infection induces autophagy in porcine placental trophoblasts (PTCs). Induction of autophagy by rapamycin (RAPA) inhibited the occurrence of apoptotic cell death, yet promoted viral replication in PPV-infected cells; inhibition of autophagy by 3-MA or ATG5 knockdown increased cellular apoptosis and reduced PPV replication. Interestingly, we found that in the presence of caspase-inhibitor zVAD-fmk, PPV induces non-apoptotic cell death that was characterized by lysosomal damage and associated with autophagy. Induction of complete autophagy flux by RAPA markedly promoted PPV replication compared with incomplete autophagy induced by RAPA plus bafilomycin (RAPA/BAF) in the early phase of PPV infection (24 h.p.i.). Meanwhile, induction of complete autophagy with RAPA increased lysosomal damage and non-apoptotic cell death in the later phase of PPV infection. Therefore, our data suggest that autophagy can enhance PPV replication and promote the occurrence of lysosomal-damage-associated non-apoptotic cell death in PPV-infected porcine placental trophoblasts.</div>
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<Abstract><AbstractText>Autophagy plays important roles in the infection and pathogenesis of many viruses, yet the regulatory roles of autophagy in the process of porcine parvovirus (PPV) infection remain unclear. Herein, we show that PPV infection induces autophagy in porcine placental trophoblasts (PTCs). Induction of autophagy by rapamycin (RAPA) inhibited the occurrence of apoptotic cell death, yet promoted viral replication in PPV-infected cells; inhibition of autophagy by 3-MA or ATG5 knockdown increased cellular apoptosis and reduced PPV replication. Interestingly, we found that in the presence of caspase-inhibitor zVAD-fmk, PPV induces non-apoptotic cell death that was characterized by lysosomal damage and associated with autophagy. Induction of complete autophagy flux by RAPA markedly promoted PPV replication compared with incomplete autophagy induced by RAPA plus bafilomycin (RAPA/BAF) in the early phase of PPV infection (24 h.p.i.). Meanwhile, induction of complete autophagy with RAPA increased lysosomal damage and non-apoptotic cell death in the later phase of PPV infection. Therefore, our data suggest that autophagy can enhance PPV replication and promote the occurrence of lysosomal-damage-associated non-apoptotic cell death in PPV-infected porcine placental trophoblasts.</AbstractText>
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	Serveur d'exploration sur la rapamycine et les champignons
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Autophagy Promotes Porcine Parvovirus Replication and Induces Non-Apoptotic Cell Death in Porcine Placental Trophoblasts.

Autophagy Promotes Porcine Parvovirus Replication and Induces Non-Apoptotic Cell Death in Porcine Placental Trophoblasts.

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