Calpain Inhibition Protects against Virus-Induced Apoptotic Myocardial Injury

DeBiasi, Roberta L.; Edelstein, Charles L.; Sherry, Barbara; Tyler, Kenneth L.

doi:10.1128/jvi.75.1.351-361.2001

Cited by 100 publications

(115 citation statements)

References 79 publications

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“…4,[32][33][34][35] We have previously shown that apoptosis is a key mechanism by which reovirus induces myocarditic cell death and tissue injury in infected animals. 4,31 We now show that in contrast to results in HEK293 cells, activation of NF-κB is not required for reovirus-induced apoptosis in primary cardiac myocytes ( Figure 6).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κ B activity and cFLIP expression contribute to viral-induced apoptosis

et al. 2005

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Virus-induced activation of nuclear factor-kappa B (NF-κB) is required for Type 3 (T3) reovirusinduced apoptosis. We now show that NF-κB is also activated by the prototypic Type 1 reovirus strain Lang (T1L), which induces significantly less apoptosis than T3 viruses, indicating that NF-κB activation alone is not sufficient for apoptosis in reovirus-infected cells. A second phase of virusinduced NF-κB regulation, where NF-κB activation is inhibited at later times following infection with T3 Abney (T3A), is absent in T1L-infected cells. This suggests that inhibition of NF-κB activation at later times post infection also contributes to reovirus-induced apoptosis. Reovirusinduced inhibition of stimulus-induced activation of NF-κB is significantly associated with apoptosis following infection of HEK293 cells with reassortant reoviruses and is determined by the T3 S1 gene segment, which is also the primary determinant of reovirus-induced apoptosis. Inhibition of stimulusinduced activation of NF-κB also occurs following infection of primary cardiac myocytes with apoptotic (8B) but not non-apoptotic (T1L) reoviruses. Expression levels of the NF-κB-regulated cellular FLICE inhibitory protein (cFLIP) reflect NF-κB activation in reovirus-infected cells. Further, inhibition of NF-κB activity and cFLIP expression promote T1L-induced apoptosis. These results demonstrate that inhibition of stimulus-induced activation of NF-κB and the resulting decrease in cFLIP expression promote reovirus-induced apoptosis.

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Section: Discussionmentioning

confidence: 99%

Inhibition of NF-κ B activity and cFLIP expression contribute to viral-induced apoptosis

et al. 2005

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“…Reovirus infection results in the release of TRAIL from infected HEK293 cells and reovirus sensitizes these cells to TRAIL-induced killing . In neonatal mice, reovirus also induces apoptosis in infected tissues in vivo (Oberhaus et al, 1997(Oberhaus et al, , 1998DeBiasi et al, 2001). However, reovirus infection is not associated with signi®cant disease in adult mice or in humans.…”

Section: Introductionmentioning

confidence: 99%

Caspase 8-dependent sensitization of cancer cells to TRAIL-induced apoptosis following reovirus-infection

et al. 2001

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“…1 ± 3 Apoptosis also plays a critical role during reovirus infection in vivo, and is the mechanism of virus-induced tissue injury in key target organs, including the central nervous system and heart. 1,4,5 Inhibition of apoptosis dramatically reduces the extent of reovirus-induced tissue injury in vivo. 5 It has been shown recently that reovirus-induced apoptosis requires interaction with its cell surface receptors including junction adhesion molecule (JAM).…”

Section: Introductionmentioning

confidence: 99%

“…1,4,5 Inhibition of apoptosis dramatically reduces the extent of reovirus-induced tissue injury in vivo. 5 It has been shown recently that reovirus-induced apoptosis requires interaction with its cell surface receptors including junction adhesion molecule (JAM). 6 Apoptosis involves the tumor necrosis factor (TNF) superfamily of cell surface death receptors, specifically DR4, DR5 and their ligand, TNF-related apoptosis-inducing ligand (TRAIL), 7 and is inhibited by anti-TRAIL antibodies or soluble forms of DR4 or DR5 which inhibit interaction of TRAIL with functional cell surface DR4 and DR5.…”

Section: Introductionmentioning

confidence: 99%

Reovirus-induced apoptosis requires both death receptor- and mitochondrial-mediated caspase-dependent pathways of cell death

2002

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Apoptosis plays an important role in the pathogenesis of many viral infections. Despite this fact, the apoptotic pathways triggered during viral infections are incompletely understood. We now provide the first detailed characterization of the pattern of caspase activation following infection with a cytoplasmically replicating RNA virus. Reovirus infection of HEK293 cells results in the activation of caspase-8 followed by cleavage of the pro-apoptotic protein Bid. This initiates the activation of the mitochondrial apoptotic pathway leading to release of cytochrome c and activation of caspase-9. Combined activation of death receptor and mitochondrial pathways results in downstream activation of effector caspases including caspase-3 and caspase-7 and cleavage of cellular substrates including PARP. Apoptosis is initiated by death receptor pathways but requires mitochondrial amplification producing a biphasic pattern of caspase-8, Bid, and caspase-3 activation.

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Calpain Inhibition Protects against Virus-Induced Apoptotic Myocardial Injury

Cited by 100 publications

References 79 publications

Inhibition of NF-κ B activity and cFLIP expression contribute to viral-induced apoptosis

Inhibition of NF-κ B activity and cFLIP expression contribute to viral-induced apoptosis

Caspase 8-dependent sensitization of cancer cells to TRAIL-induced apoptosis following reovirus-infection

Reovirus-induced apoptosis requires both death receptor- and mitochondrial-mediated caspase-dependent pathways of cell death

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