Programmed Necrotic Cell Death Induced by Complement Involves a Bid-Dependent Pathway

Ziporen, Lea; Donin, Natalie; Shmushkovich, Taisia; Gross, Atan; Fishelson, Zvi

doi:10.4049/jimmunol.182.1.515

Cited by 35 publications

(28 citation statements)

References 43 publications

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“…However, recent literature argues that necrosis is a result of a well-orchestrated interplay of signalling cascades, 27 with an extensive crosstalk between biochemical and molecular events. 28,29 Furthermore, some signalling molecules, which play a role in autophagy and apoptosis, also take part in this interplay. 30 A cell may show morphological or molecular features characteristic of autophagy, apoptosis or necrosis without having completely lost membrane integrity, having undergone complete nuclear fragmentation or having been engulfed by a neighboring cell.…”

Section: Dynamics Within Modes Of Cell Deathmentioning

confidence: 99%

Cell death: A dynamic response concept

Loos

Engelbrecht²

2009

Autophagy

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Autophagy, apoptosis and necrosis have previously been described as distinct static processes that induce and execute cell death. Due to an increased use of novel techniques in mapping cellular death-techniques which allow for reporting of real-time data-the existence of "grey zones" between cell death modes and the existence of the "point of no return" within these have been revealed. This revelation demands the integration of new concepts in describing the cellular death process. Furthermore, since the contribution of autophagy in cell death or cell survival is still poorly understood, it is important to accurately describe its function within the dynamic framework of cell death.In this review cell death is viewed as a dynamic and integrative cellular response to ensure the highest likelihood of self-preservation. Suggestions are offered for conceptualizing cell death modes and their morphological features, both individually and in relation to one another. It addresses the need for distinguishing between dying cells and dead cells so as to better locate and control the onset of cell death. Most importantly, the fundamental role of autophagy, autophagic flux, and the effects of the intracellular metabolic environment on the kinetics of the cell death modes are stressed. It also contextualizes the kinetic dimension of cell death as a process and aims to contribute towards a better understanding of autophagy as a key mechanism within this process. Understanding the dynamic nature of the cell death process and autophagy's central role can reveal new insight for therapeutic intervention in preventing cell death.

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Section: Dynamics Within Modes Of Cell Deathmentioning

confidence: 99%

Cell death: A dynamic response concept

Loos

Engelbrecht²

2009

Autophagy

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“…At least to some extent, the necrotic cell death inflicted by the C5b-9 complex is programmed and involves Bid and JNK (6,7). Some of the death signals are counteracted by ERK (9).…”

Section: Discussionmentioning

confidence: 99%

“…10), this is not surprising. Bid is involved in necrotic cell death activated by both C5b-9 and SLO (6). Unlike C5b-9, SLO does not induce JNK activation (7).…”

Section: Discussionmentioning

confidence: 99%

“…Cell lysis by complement (NHS) was measured by the PI and trypan blue inclusion methods as described before (6). Both methods measure plasma membrane damage and permeability and were used interchangeably.…”

Section: Cytotoxicity Assaysmentioning

confidence: 99%

“…The membrane inserted C5b-9 complexes can transmit various signals into target cells (2). Activation of JNK and BH3 interacting domain death agonist (Bid) promotes cell death (6,7). In contrast, activation of protein kinase C and ERK supports cell protection from complement-dependent cytotoxicity (8,9).…”

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confidence: 99%

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A Role for the NF-κB Pathway in Cell Protection from Complement-Dependent Cytotoxicity

Gancz

Lusthaus

Fishelson

2012

The Journal of Immunology

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Nucleated cells are equipped with several mechanisms that support their resistance to complement-dependent cytotoxicity (CDC). The role of the NF-κB pathway in cell protection from CDC was examined. Elevated sensitivity to CDC was demonstrated in cells lacking the p65 subunit of NF-κB or the IκB kinases IKKα or IKKβ, and in cells treated with p65 small interfering RNA. Pretreatment with the IKK inhibitor PS-1145 also enhanced CDC of wild-type cells (WT) but not of p65−/− cells. Furthermore, reconstitution of p65 into p65−/− cells and overexpression of p65 in WT cells lowered their sensitivity to CDC. The postulated effect of p65 on the JNK-mediated death-signaling pathway activated by complement was examined. p65 small interfering RNA enhanced CDC in WT cells but not in cells lacking JNK. JNK phosphorylation induced by complement was more pronounced in p65−/− cells than in WT cells. The results indicate that the NF-κB pathway mediates cell resistance to CDC, possibly by suppressing JNK-dependent programmed necrotic cell death.

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Differential proteomic analysis of synovial fluid from hip arthroplasty patients with a pseudotumor vs. Periprosthetic osteolysis

Catelas

Lehoux

Ning

et al. 2018

Journal Orthopaedic Research

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Adverse tissue reactions to metal implants, including pseudotumors, can compromise implant functionality and survivorship. The identification of specific proteins in the synovial fluid (SF) of hip arthroplasty patients with a pseudotumor may lead to a better understanding of the underlying pathomechanisms. The objective of the present study was to compare the protein content of SF from patients with a short-term metal-on-metal hip implant associated with a pseudotumor and patients with a long-term metal-on-polyethylene hip implant associated with periprosthetic osteolysis. Discovery proteomics was used to identify differentially abundant proteins in albumin-depleted SF. In toto, 452 distinct proteins (present in at least half of the patients in one or both groups) were identified. Thirty of these 452 proteins were differentially abundant between the two groups, including two potential biomarkers: 6-phosphogluconate dehydrogenase (which plays a major protective role against oxidative stress) for the pseudotumor group, and scavenger receptor cysteine-rich type 1 protein M130 (which is involved in low-grade inflammation) for the periprosthetic osteolysis group. Other differentially abundant proteins identified suggest the presence of an adaptive immune response (particularly a type-IV hypersensitivity reaction), necrosis, and greater oxidative stress in patients with a pseudotumor. They also suggest the presence of an innate immune response, oxidative stress, tissue remodeling, and apoptosis in both patient groups, although differences in the specific proteins identified in each group point to differences in the pathomechanisms. Overall, results provide insights into the molecular mechanisms underlying metal-related pseudotumors and periprosthetic osteolysis, and may ultimately help elucidate pseudotumor etiology and assess the risk that asymptomatic pseudotumors will develop into an aggressive lesion. © 2018 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 36:1849-1859, 2018.

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Programmed Necrotic Cell Death Induced by Complement Involves a Bid-Dependent Pathway

Cited by 35 publications

References 43 publications

Cell death: A dynamic response concept

Cell death: A dynamic response concept

A Role for the NF-κB Pathway in Cell Protection from Complement-Dependent Cytotoxicity

Differential proteomic analysis of synovial fluid from hip arthroplasty patients with a pseudotumor vs. Periprosthetic osteolysis

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