Role of BNIP3 in TNF-induced cell death — TNF upregulates BNIP3 expression

Ghavami, Saeid; Eshraghi, Mehdi; Kadkhoda, Kamran; Mutawe, Mark M.; Maddika, Subbareddy; Bay, Graham H.; Wesselborg, Sebastian; Halayko, Andrew J.; Klonisch, Thomas; Łos, Marek

doi:10.1016/j.bbamcr.2009.01.002

Cited by 60 publications

(50 citation statements)

References 76 publications

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“…As a serine protease, cathepsin is known to induce cellular autolysis and damage of neighboring cells during necrosis [52]. However, many lines of evidence show that lysosomal cathepsin plays an additional role in cell death pathways activated by various stimuli, including BNip3 [7,53]. While it is clear that lysosomes play a significant role in cell death caused by BNip3 overexpression, the target protein responsible for the propagation of cell death is not clearly identified.…”

Section: Discussionmentioning

confidence: 98%

BNip3 is a mediator of TNF-induced necrotic cell death

Kim

Lee

et al. 2010

Apoptosis

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Tumor necrosis factor (TNF) is a pleiotropic cytokine involved in immune modulation, inflammatory reactions, and target cell death in many pathologic conditions. The cell death pathways triggered by TNF include the caspase-8/Bid-dependent apoptotic pathway and the caspase-independent necrosis pathway (necroptosis). While the signaling pathways activated after binding of TNF to the TNF receptor (TNFR) and subsequent insertion of Bid/Bax/Bik into the outer mitochondrial membrane are relatively well known, other cell death pathways and the participating signaling molecules remain to be clarified. BNip3 is a pro-death protein and a member of the BH3-only Bcl-2 family. When ectopically overexpressed or induced by hypoxia, BNip3 induces various types of cell death via mitochondrial or non-mitochondrial death cascades. In this study using A549 alveolar epithelial cells of the lung, we show that BNip3 is transcriptionally and translationally upregulated by TNF, and its expression level determines the sensitivity to necroptosis induced by TNF. However, BNip3 does not appear to be involved in caspase-8/Bid-dependent apoptotic cell death in these alveolar lung cells. Finally, we show that the generation of reactive oxygen species (ROS) is essential for mitochondrial insertion of BNip3, which is an important step in BNip3-induced mitochondrial catastrophe. Our results indicate that BNip3 is a candidate therapeutic target in pathologic conditions in which TNF causes tissue damage.

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Section: Discussionmentioning

confidence: 98%

BNip3 is a mediator of TNF-induced necrotic cell death

Kim

Lee

et al. 2010

Apoptosis

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“…One possibility is that cathepsin B is upstream of ROS production in response to many stimuli. A known role for cathepsin B in caspase-independent mitochondrial membrane destabilization and subsequent oxidative stress has been reported (15,16,47,50,58), although not necessarily in the context of the prosurvival NF-B activation.…”

Section: Discussionmentioning

confidence: 99%

Adenovirus Membrane Penetration Activates the NLRP3 Inflammasome

Barlan

Griffin

McGuire

et al. 2011

J Virol

153

161

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Adenovirus type 5 (Ad5) infection of macrophages results in rapid secretion of interleukin-1␤ (IL-1␤) and is dependent on the inflammasome components NLRP3 and ASC and the catalytic activity of caspase-1. Using lentivirus-expressed short hairpin RNA (shRNA) and competitive inhibitors, we show that Ad-induced IL-1␤ release is dependent upon Toll-like receptor 9 (TLR9) sensing of the Ad5 double-stranded DNA (dsDNA) genome in human cell lines and primary monocyte-derived macrophages but not in mouse macrophages. Additionally, a temperature-sensitive mutant of Ad5 unable to penetrate endosomal membranes, ts1, is unable to induce IL-1␤ release in TLR2-primed THP-1 cells, suggesting that penetration of endosomal membranes is required for IL-1␤ release. Disruption of lysosomal membranes and the release of cathepsin B into the cytoplasm are required for Ad-induced NLRP3 activation. Ad5 cell entry also induces reactive oxygen species (ROS) production, and inhibitors of ROS prevent Ad-induced IL-1␤ release. Ad5 activation of NLRP3 also induces necrotic cell death, resulting in the release of the proinflammatory molecule HMGB1. This work further defines the mechanisms of virally induced inflammasome activation.

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“…Functionally well-known member of caspase family, caspase-8, is crucial factor for TNF-induced extrinsic apoptotic pathway [51]. Pro-caspase-8 is recruited to DISC by FADD, and dimerization or trimerization triggers pro-caspase-8 activation via reciprocal cleavage.…”

Section: Caspase Family Membersmentioning

confidence: 99%

Major apoptotic mechanisms and genes involved in apoptosis

et al. 2016

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As much as the cellular viability is important for the living organisms, the elimination of unnecessary or damaged cells has the opposite necessity for the maintenance of homeostasis in tissues, organs and the whole organism. Apoptosis, a type of cell death mechanism, is controlled by the interactions between several molecules and responsible for the elimination of unwanted cells from the body. Apoptosis can be triggered by intrinsically or extrinsically through death signals from the outside of the cell. Any abnormality in apoptosis process can cause various types of diseases from cancer to auto-immune diseases. Different gene families such as caspases, inhibitor of apoptosis proteins, B cell lymphoma (Bcl)-2 family of genes, tumor necrosis factor (TNF) receptor gene superfamily, or p53 gene are involved and/or collaborate in the process of apoptosis. In this review, we discuss the basic features of apoptosis and have focused on the gene families playing critical roles, activation/inactivation mechanisms, upstream/downstream effectors, and signaling pathways in apoptosis on the basis of cancer studies. In addition, novel apoptotic players such as miRNAs and sphingolipid family members in various kind of cancer are discussed.

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Role of BNIP3 in TNF-induced cell death — TNF upregulates BNIP3 expression

Cited by 60 publications

References 76 publications

BNip3 is a mediator of TNF-induced necrotic cell death

BNip3 is a mediator of TNF-induced necrotic cell death

Adenovirus Membrane Penetration Activates the NLRP3 Inflammasome

Major apoptotic mechanisms and genes involved in apoptosis

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