Caspase activation in equine influenza virus induced apoptotic cell death

Lin, Chengbin; Holland, Robert E.; Donofrio, Jennifer C.; McCoy, Morgan H.; Tudor, Lynn R.; Chambers, Thomas M.

doi:10.1016/s0378-1135(01)00468-0

Cited by 49 publications

(27 citation statements)

References 30 publications

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“…We further evaluated the activation of the apoptotic pathway downstream of Bax. The cleaved 84-kDa form of PARP is known to be generated by activated caspase-3 (49) and to be increased by influenza virus infection (23,32). In support of Bax regulation, the level of cleaved PARP markedly increased in HEK cells at 2 dpi, but not in SPL cells (Fig.…”

Section: S1p Lyase Overexpression Inhibits Influenza Virus Propagatiomentioning

confidence: 74%

Sphingosine 1-Phosphate-Metabolizing Enzymes Control Influenza Virus Propagation and Viral Cytopathogenicity

Seo¹,

Blake²,

Alexander

et al. 2010

J Virol

104

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Sphingosine 1-phosphate (S1P)-metabolizing enzymes regulate the level of sphingolipids and have important biological functions. However, the effects of S1P-metabolizing enzymes on host defense against invading viruses remain unknown. In this study, we investigated the role of S1P-metabolizing enzymes in modulating cellular responses to influenza virus infection. Overexpression of S1P lyase (SPL), which induces the degradation of S1P, interfered with the amplification of infectious influenza virus. Accordingly, SPL-overexpressing cells were much more resistant than control cells to the cytopathic effects caused by influenza virus infection. SPL-mediated inhibition of virus-induced cell death was supported by impairment of the upregulation of the proapoptotic protein Bax, a critical factor for influenza virus cytopathogenicity. Importantly, influenza virus infection of SPL-overexpressing cells induced rapid activation of extracellular signal-regulated kinase (ERK) and STAT1 but not of p38 mitogen-activated protein kinase (MAPK), Akt, or c-Jun N-terminal kinase (JNK). Blockade of STAT1 expression or inhibition of Janus kinase (JAK) activity elevated the level of influenza virus replication in the cells, indicating that SPL protects cells from influenza virus via the activation of JAK/STAT signaling. In contrast to that of SPL, the overexpression of S1P-producing sphingosine kinase 1 heightened the cells' susceptibility to influenza virus infection, an effect that was reversed by the inhibition of its kinase activity, representing opposed enzymatic activity. These findings indicate that the modulation of S1P-metabolizing enzymes is crucial for controlling the host defense against infection with influenza virus. Thus, S1P-metabolizing enzymes are novel potential targets for the treatment of diseases caused by influenza virus infection.

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Section: S1p Lyase Overexpression Inhibits Influenza Virus Propagatiomentioning

confidence: 74%

Sphingosine 1-Phosphate-Metabolizing Enzymes Control Influenza Virus Propagation and Viral Cytopathogenicity

Seo¹,

Blake²,

Alexander

et al. 2010

J Virol

104

View full text Add to dashboard Cite

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“…Such cleavage events may result in important alterations to normal homeostatic cellular processes. (56) PARP has been shown to be a cellular target of caspase-3 and other caspases. In AGS cells, after 72-h transfection with TRPM7siRNA, PARP becomes proteolytically cleaved from a 116-kDa intact form into 85-kDa fragments (Fig.…”

Section: Discussionmentioning

confidence: 99%

Suppression of transient receptor potential melastatin 7 channel induces cell death in gastric cancer

et al. 2008

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CaAmong ion channels, the transient receptor potential (TRP) melastatin 6 and 7 channel is similarly permeable to both of the dominant divalent cations Ca 2+ and Mg 2+ .(4) TRP channels were first cloned from the Drosophila species (TRP and transient receptor potential-like protein) and constitute a superfamily of proteins that encode a diverse group of Ca 2+ -permeable nonselective cation channels.(5) The TRP family is divided into three subfamilies: classic, vanilloid (TRPV), and melastatin type (TRPM).(5) The eight TRPM family members differ significantly from other TRP channels in terms of domain structure, cation selectivity, and activation mechanisms.(5) By mediating cation entry as well as membrane depolarization, activation of the TRPM subfamily of ion channels has a profound influence on various physiologic and pathologic processes. (6,7) TRPM7 is endogenously expressed in a wide variety of tissues including brain and hematopoietic tissues (8) as well as kidney and heart tissues.(9-11) The TRPM7 cation channel supports multiple cellular and physiological functions, including cellular Mg 2+ homeostasis, (12,13) cell viability and growth, (13)(14)(15)(16) anoxic neuronal cell death, (17) synaptic transmission, (18) cell adhesion, (19,20) and intestinal pacemaking.(21) Recently, Wykes et al. (22) suggested that TRPM7 channels are critical for human mast cell survival, and Jiang et al. (23) suggested that activation of TRPM7 channels is critical for the growth and proliferation of human head and neck carcinoma cells. Also Abed et al. (24) proposed the importance of TRPM7 in human osteoblast-like cell proliferation. However, the presence and potential function of TRPM7 channels in human gastric cancer cells are unknown.In this study, we examined the presence and potential role of TRPM7 channels in the growth and survival of AGS cells, the most common human gastric adenocarcinoma cell line. Our data suggest that TRPM7 channels have an important role in the survival of these tumor cells. Materials and MethodsCells. Five human gastric adenocarcinoma cell lines (AGS, MKN-1, MKN-45, SNU-1, and SNU-484) were used. Among them, we used mainly AGS cell line, the most common human gastric adenocarcinoma cell line. All cell lines were established at

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“…In influenza virus-infected cells, caspases are implicated in various cellular functions, such as apoptotic cell degradation [25,26] , the post-transcriptional processing of cellular cytokine and viral component proteins [27,28] , and efficient virus proliferation [29] . Caspase-3 plays a key role for apoptotic cell degradation, and the cleavage of pro-caspase-3 protein into active forms is an essential process for apoptotic cell degradation induced by various stimuli [30] .…”

Section: Introductionmentioning

confidence: 99%

Lactate Dehydrogenase Leakage as a Marker for Apoptotic Cell Degradation Induced by Influenza Virus Infection in Human Fetal Membrane Cells

et al. 2009

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Objective: In order to elucidate the implication of apoptosis in lactate dehydrogenase (LDH) leakage from influenza virus-infected cells, the effects of a general caspase inhibitor, N-t-Boc-Asp(OMe)-fluoromethylketone (Boc-D-fmk), on LDH leakage, apoptosis induction and virus proliferation were examined. Methods: Cultured human fetal membrane chorion and amnion cells were incubated with or without Boc-D-fmk after influenza virus infection. LDH leakage was estimated by measuring LDH activities in the culture supernatants and cell lysates. The extent of apoptosis was determined by caspase-3 protein cleavage and DNA fragmentation. Virus proliferation was determined by a plaque-forming assay. Results: While virus proliferation was observed in both chorion and amnion cells, the virus infection resulted in LDH leakage, caspase-3 protein cleavage, and oligonucleosomal DNA fragmentation, all of which were observed only in the chorion cells and inhibited by the presence of Boc-D-fmk except for the virus proliferation. Conclusion: LDH level in amniotic fluid is known to be one of markers for predicting fetal membrane damage. Therefore, this study provides a possible diagnostic application of LDH level to predict the extent of tissue damage of fetal membranes via apoptosis induced by influenza virus infection.

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Caspase activation in equine influenza virus induced apoptotic cell death

Cited by 49 publications

References 30 publications

Sphingosine 1-Phosphate-Metabolizing Enzymes Control Influenza Virus Propagation and Viral Cytopathogenicity

Sphingosine 1-Phosphate-Metabolizing Enzymes Control Influenza Virus Propagation and Viral Cytopathogenicity

Suppression of transient receptor potential melastatin 7 channel induces cell death in gastric cancer

Lactate Dehydrogenase Leakage as a Marker for Apoptotic Cell Degradation Induced by Influenza Virus Infection in Human Fetal Membrane Cells

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