About: Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation

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About: Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation
Creator	Zhang, Liang Huang, Yong Tong, Dewen Zhao, Xiaomin Song, Xiangjun Xiang, Hailing Bai, Xiaoyuan Fei, Naijiao Zhang, Hongling
Source	Medline; PMC
abstract	BACKGROUND: Porcine parvovirus (PPV) infection primarily causes reproductive failure of pregnant swine and results in host cell death. Boars, as an important disseminator, shed PPV to sows via semen. PPV infects and numerously replicates in boar testicle, which results in damage of swine testicle in vivo. Reactive oxygen species (ROS), a mediator of cell apoptosis, play a crucial role in the mitochondria apoptotic pathway. However, whether PPV infection induces ST cells apoptosis and ROS accumulation is still unclear. METHODS: To determine the effects of PPV infection on the apoptosis, we detected morphological changes, DNA ladder, activities of caspases, and expression of PARP in PPV-infected ST cells. Moreover, aiming to investigate the effect of PPV infection on the mitochondrial apoptotic pathway and ROS accumulation, we detected the Δψm, apoptosis-related genes, and ROS. To investigate the role of ROS in the process of PPV-induced apoptosis, the ST cells were infected with PPV and treated with the ROS antioxidants. The ROS level was measured using Reactive Oxygen Species Assay Kit and the Δψm, expression level of Bcl-2, translocation of Bax, and redistribution of mitochondria cytochrome c were tested. RESULTS: In this study, we demonstrated that PPV infection could induce apoptosis that was characterized by morphological changes, DNA fragmentation and activation of caspases. Moreover, PPV infection suppressed Bcl-2 expression, enhanced Bax expression and translocation to mitochondria, decreased the mitochondrial transmembrane potential, and triggered the release of cytochrome c, which caused the subsequent activation of caspase-9 and caspase-3 and initiation of apoptosis. However, during the process of PPV-induced apoptosis, the protein levels of Fas and FasL were not affected. Further studies showed that PPV infection caused ROS accumulation. Inhibition of ROS could reduce mitochondrial transmembrane potential and could significantly block ST cells apoptosis via suppressing Bax translocation, cytochrome c and caspase-3 activation. CONCLUSIONS: All these results suggest that PPV-induced ROS accumulation mediates apoptosis in ST cells, which provided theoretical basis for the molecular pathogenesis of PPV infection.
has issue date	2016-02-16(xsd:dateTime)
bibo:doi	10.1186/s12985-016-0480-z
bibo:pmid	26880103
has license	cc-by
sha1sum (hex)	8e3f518b27782ac9cc19e7556d74100ff23d972b
schema:url	https://doi.org/10.1186/s12985-016-0480-z
resource representing a document's title	Porcine parvovirus infection activates mitochondria-mediated apoptotic signaling pathway by inducing ROS accumulation
has PubMed Central identifier	PMC4755023
has PubMed identifier	26880103
schema:publication	Virol J
resource representing a document's body	covid:8e3f518b27782ac9cc19e7556d74100ff23d972b#body_text
is schema:about of	named entity 'apoptosis' named entity 'level' named entity 'tested' named entity 'apoptotic' named entity 'infection' covid:arg/8e3f518b27782ac9cc19e7556d74100ff23d972b named entity 'infection' named entity 'vivo' named entity 'Bax' named entity 'replicates' named entity 'cell' named entity 'boar' named entity 'determine' named entity 'cells' named entity 'PPV' named entity 'non-fat dry milk' named entity 'parvovirus' named entity 'ROS' named entity 'caspase-9' named entity '37°C' named entity 'Bax' named entity 'tissue culture' named entity 'fetal' named entity 'infection' named entity 'infection' named entity 'ROS' named entity 'cytoplasm' named entity 'mitochondrial potential' named entity 'ROS' named entity 'caspases' named entity 'ROS' named entity 'apoptotic' named entity 'permeabilization' named entity 'apoptosis' named entity 'infection' named entity 'translocation' named entity 'PBS' named entity 'cytochrome' named entity 'Apoptosis' named entity '37°C' named entity 'mitochondria' named entity 'total protein' named entity 'adaptor molecules' named entity 'translocation' named entity 'mitochondrial oxidation' named entity 'extrinsic apoptotic pathway' named entity 'virus' named entity 'Bax' named entity 'ROS' named entity 'depolarized' named entity 'chromatin condensation' named entity 'canine parvovirus' named entity 'TNFR' named entity 'caspase-3' named entity 'Apoptosis' named entity 'ROS' named entity 'lysis buffer' named entity 'hpi' named entity 'Bax' named entity 'caspase-3' named entity 'ROS' named entity 'apoptosis' named entity 'mitochondrial membrane potential' named entity 'Bax' named entity 'involved in the formation' named entity 'caspase-8' named entity 'infection' named entity 'caspase-3' named entity 'ROS' named entity 'ROS' named entity 'caspase' named entity 'western blot' named entity 'Promega Corporation'

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