Anti-apoptotic genes Bcl-2 and Bcl-xL overexpression can block iridovirus serine/threonine kinase-induced Bax/mitochondria-mediated cell death in GF-1 cells

Reshi, Latif; Wang, Hua-Ven; Hui, Cho-Fat; Su, Y. K.; Hong, Jiann Ruey

doi:10.1016/j.fsi.2016.12.026

Cited by 37 publications

(31 citation statements)

References 55 publications

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“…Although Bax is mainly located in the cytoplasm, when stimulated, it can move closer to the mitochondrial membrane (42). When Bax converges onto the mitochondria, combining with other pro-apoptotic Bcl-2 family members, it induces the release of cytochrome c through the pore channels formed in the outer membrane of the mitochondria by oligomerization or by other channels (43)(44)(45). Phosphorylation of JNK and p38 MAPK activates Bax, either alone or in combination (46).…”

Section: Discussionmentioning

confidence: 99%

Methyl ferulic acid exerts anti-apoptotic effects on L-02 cells via the ROS-mediated signaling pathway

Zhong

et al. 2018

Int J Oncol

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The present study aimed to investigate the anti-apoptotic effects of methyl ferulic acid (MFA) on L-02 cell apoptosis induced by ethanol, and to elucidate the possible underlying mechanisms. L-02 cells were examined after being soaked in ethanol (400 mM) to allow the ethanol to permeate into the cells for 24 h. Cell survival was measured by MTT assay. Cell apoptosis was assessed by both flow cytometry and single-stranded DNA assays. Intracellular reactive oxygen species (ROS) production was determined using the 2',7'-dichlorofluorescein-diacetate dye. The protein expression levels of p38, p-p38, JNK, p-JNK, NADPH oxidase 4 (NOX4), p22, Bax and Bcl-2 were measured by western blot analysis. The mRNA expression levels of NOX4 and p22 were measured by RT-PCR. It was identified that MFA markedly suppressed the ethanol-induced apoptosis and necrosis of L-02 cells. In addition, MFA decreased the expression levels of superoxide dismutase, catalase and phospholipid hydroperoxide gluthione peroxidase, and downregulated the levels of Bax/Bcl-2 and the cleaved forms of caspase-3 in a dose- and time-dependent manner. This indicated that MFA attenuated the apoptosis of L-02 cells. MFA also decreased the elevated mRNA and protein expression levels of Nox4 and p22phox, and the production of intracellular ROS triggered by ethanol. Further analysis demonstrated that MFA significantly attenuated the phosphorylation of JNK and p38, which are major components of the mitogen-activated protein kinase (MAPK) pathways. On the whole, the findings of this study demonstrated that MFA attenuated the apoptotic cell death of L-02 cells by reducing the generation of ROS and inactivating the MAPK pathways.

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Section: Discussionmentioning

confidence: 99%

Methyl ferulic acid exerts anti-apoptotic effects on L-02 cells via the ROS-mediated signaling pathway

Zhong

et al. 2018

Int J Oncol

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“…Therefore, the increased expression levels of Bim, Bax, and Bak corresponded to those of cytosolic Cyt c and Endo G in this study. Nevertheless, the antiapoptotic Bcl-2 and Bcl-xl have been reported to inhibit apoptosis by binding to Bax or Bak [50], thereby preventing the release of Cyt c and subsequent caspase activation [49]. Kawakami and colleagues [51] have found that a high intake of Cu can induce apoptosis via increasing the expression levels of Bax, Bad, caspase-3, Cyt c, and caspase-9 in PC12 cells.…”

Section: Procaspase-9mentioning

confidence: 99%

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Liu

Guo

Jian

et al. 2020

Oxidative Medicine and Cellular Longevity

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Copper (Cu) is an essential trace element involved in the normal physiological processes of animals. However, excessive exposure to Cu can produce numerous detrimental impacts. The aim of this study was to investigate the effects of Cu on oxidative stress and apoptosis as well as their relationship in the mouse liver. Four-week-old ICR mice (n=240) were randomly assigned to different Cu (Cu2+-CuSO4) treatment groups (0, 4, 8, and 16 mg/kg) for periods of 21 and 42 days. The high doses of Cu exposure could induce oxidative stress, by increasing the levels of reactive oxygen species (ROS) and protein carbonyls (PC) and decreasing the activities of antisuperoxide anion (ASA) and antihydroxyl radical (AHR) and content of glutathione (GSH), as well as activities and mRNA expression levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Moreover, high doses of Cu exposure induced hepatic apoptosis via the mitochondrial apoptotic pathway, as characterized by the depolarization of mitochondrial membrane potential (MMP); significantly increased mRNA and protein expression levels of cytosolic cytochrome (Cyt c), apoptosis-inducing factor (AIF), endonuclease G (Endo G), apoptosis protease-activating factor-1 (Apaf-1), cleaved caspase-9, cleaved caspase-3, cleaved PARP, Bcl-2 antagonist killer (Bak), Bcl-2-associated X protein (Bax), and Bcl-2-interacting mediator of cell death (Bim); and decreased mRNA and protein expression levels of B-cell lymphoma-2 (Bcl-2) and Bcl-extra-large (Bcl-xL). Furthermore, the activation of the tumor necrosis factor receptor-1 (TNF-R1) signaling pathway was involved in Cu-induced apoptosis, as characterized by the significantly increased mRNA and protein expression levels of TNF-R1, Fas-associated death domain (FADD), TNFR-associated death domain (TRADD), and cleaved caspase-8. These results indicated that exposure to excess Cu could cause oxidative stress triggered by ROS overproduction and diminished antioxidant function, which in turn promoted hepatic apoptosis via mitochondrial apoptosis and that the TNF-R1 signaling pathway was also involved in the Cu-induced apoptosis.

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“…The mechanism of DNA virus-induced nonapoptotic cell death is not well understood. Although not all signaling pathways that induce apoptosis are fully understood, the fate of a cell undergoing apoptosis mainly depends on the balance between the Bcl-2 family sensor proteins, which can promote and inhibit apoptosis (Figure 1) [9][10][11]. Recent studies have shown viral pathogenesis that involves oxidative damage and apoptosis.…”

Section: Intrinsic and Extrinsic Pathways Of Apoptosis In Viral Infecmentioning

confidence: 99%

“…Recent studies have shown that mitochondria are the targets of the reactive oxygen species (ROS) that are produced inside a cell during viral infections, and that mtDNA is a major target of these ROS [11]. Mitochondrial ATP generation requires proteins from the nuclear and mitochondrial genomes.…”

Section: Role Of Ros In Viral Diseasesmentioning

confidence: 99%

“…[2], is activation of Fas death receptors at the cell surface by its ligand for activating the caspase-8 for either cleaved Bid to tBid for targeting into mitochondria [24] or activates the ROS/RIP3mediated necroptosis via a nonmitochondria-mediated cell death process [2,85]. In the intrinsic apoptosis pathway (top left), some death factors trigger death signals on disrupting mitochondrial function via loss of MMP and release the cytochrome c and activate the downstream caspase-3 for further triggering apoptotic cell death, but these mitochondriamediated death signaling also regulated by anti-apoptotic family members such as Bcl-2 and Bcl-xL for rescuing host cells [8,10,11,87]. On the other hand, IAP can inhibit the caspase-3 activation [88] but it is suppressed by the Smac/ DIABLO molecule, which is released from mitochondria [24].…”

Section: Role Of Ros In Viral Diseasesmentioning

confidence: 99%

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Modulation of Mitochondria During Viral Infections

Reshi¹,

Wang²,

Hong³

2018

Mitochondrial Diseases

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Mitochondria are organelles critical for cell survival because they produce ATP and modulate programmed cell death (PCD) pathways. PCD pathways are important in many clinical disorders, such as ischemia/reperfusion injuries, trauma, and toxic/metabolic syndromes, as well as in chronic neurodegenerative conditions, such as amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, and Huntington's disease. Moreover, many viruses and other pathogens target the mitochondria. Viruses induce the production of various proteins in their hosts that have proapoptotic and anti-apoptotic activities, depending on the cellular environment. More specifically, many viruses that target mitochondria regulate the balance between the anti-and proapoptotic Bcl-2 family proteins and thereby increase their own survival within the host cell. Recent studies indicated that mitochondria centralize several critical innate immune responses based on the presence of several important signaling proteins within the mitochondria: mitochondrial antiviral signaling (MAVS), stimulation of interferon genes (STING), and NLR family member X1. Therefore, mitochondria are not only vital because they regulate cell survival and death but also they have broad roles in the control of cell functions following pathogen invasion. This chapter highlights the tight interplay between viral infection and mitochondria.

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Anti-apoptotic genes Bcl-2 and Bcl-xL overexpression can block iridovirus serine/threonine kinase-induced Bax/mitochondria-mediated cell death in GF-1 cells

Cited by 37 publications

References 55 publications

Methyl ferulic acid exerts anti-apoptotic effects on L-02 cells via the ROS-mediated signaling pathway

Methyl ferulic acid exerts anti-apoptotic effects on L-02 cells via the ROS-mediated signaling pathway

Copper Induces Oxidative Stress and Apoptosis in the Mouse Liver

Modulation of Mitochondria During Viral Infections

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