2007
DOI: 10.1007/s10495-007-0089-1
|View full text |Cite
|
Sign up to set email alerts
|

Mitochondrion-mediated apoptosis induced by Rana grylio virus infection in fish cells

Abstract: A fish cell line, fathead minnow (FHM) cell, was used to investigate the alteration of mitochondrial dynamics and the mechanism of apoptosis under Rana grylio virus (RGV) infection. Microscopy observations, flow-cytometry analysis and molecular marker detection revealed the apoptotic fate of the RGV-infected cells. Some typical apoptotic characteristics, such as chromatin condensation, DNA fragmentation and mitochondrial fragmentation, were observed, and significantly morphological changes of mitochondria, inc… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
2

Citation Types

5
37
0
2

Year Published

2007
2007
2024
2024

Publication Types

Select...
4
2

Relationship

2
4

Authors

Journals

citations
Cited by 64 publications
(44 citation statements)
references
References 37 publications
5
37
0
2
Order By: Relevance
“…Iridovirus-induced apoptosis is likely mediated by cellular caspases since Z-VAD-FMK, a pan-caspase inhibitor, blocks apoptosis Paul et al 2007). In addition, Huang et al (2007a) reported mitochondrial fragmentation, the activation of caspases 3 and 9, and an increase in intracellular Ca +2 in RGV-infected cells. Although it is not known whether apoptosis is a consequence of PKR activation, translational shutoff, or occurs independently of those events, Paul et al (2007) demonstrated that the amount of soluble virion extract required to induce apoptosis was 1,000-fold lower than the dose required to shutdown protein synthesis.…”
Section: Apoptosismentioning
confidence: 99%
See 1 more Smart Citation
“…Iridovirus-induced apoptosis is likely mediated by cellular caspases since Z-VAD-FMK, a pan-caspase inhibitor, blocks apoptosis Paul et al 2007). In addition, Huang et al (2007a) reported mitochondrial fragmentation, the activation of caspases 3 and 9, and an increase in intracellular Ca +2 in RGV-infected cells. Although it is not known whether apoptosis is a consequence of PKR activation, translational shutoff, or occurs independently of those events, Paul et al (2007) demonstrated that the amount of soluble virion extract required to induce apoptosis was 1,000-fold lower than the dose required to shutdown protein synthesis.…”
Section: Apoptosismentioning
confidence: 99%
“…As with CPE, apoptosis is triggered following either productive infection or treatment with heat-inactivated or UV-inactivated virus or a soluble virion extract (Essbauer and Ahne 2002;Chinchar et al 2003;Hu et al 2004;Imajoh et al 2004;Paul et al 2007;Huang et al 2007a). In FV3-infected cells, apoptosis begins 6-8 h postinfection (p.i.)…”
Section: Apoptosismentioning
confidence: 99%
“…Moreover, previous studies have revealed that STIV and FV3 can propagate in fish cells and evoke an obvious cytopathic effect (CPE), which is characterized by drastic cell rounding and cell death [1,2]. Typical apoptosis is induced by iridovirus infection, including FV3, Rana grylio virus (RGV), and Chilo iridescent virus (CIV) [4][5][6], and it has been shown for CIV that c-Jun N-terminal kinase (JNK) is required for apoptosis [6]. However, it is not known whether these or other intracellular signaling pathways are involved in iridovirus replication.…”
Section: Introductionmentioning
confidence: 99%
“…To date, some genes of RGV have been identified and characterized, such as 3b-hydroxysteroid dehydrogenase (3b-HSD), deoxyuridine triphosphatase (dUTPase), an envelope protein gene (53R), thymidine kinase (TK) and a gene belonging to the ''essential for respiration and viability'' family (ERV1) [19][20][21][22][23][24]. We found that RGV could induce apoptosis mediated by mitochondria [25]. RGV has the potential to be used as a viral vector for expression of foreign genes in fish cells [26].…”
mentioning
confidence: 99%