Necroptosis, in vivo detection in experimental disease models

Jouan-Lanhouet, Sandrine; Riquet, Franck B.; Duprez, Linde; Berghe, Tom Vanden; Takahashi, Nozomi; Vandenabeele, Peter

doi:10.1016/j.semcdb.2014.08.010

Cited by 147 publications

(131 citation statements)

References 167 publications

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“…Interestingly, our model of regulated cell death induced by 5-aminolevulinic acid-based PDT in LN-18 glioblastoma cells can be considered as a rare cellular model where necroptosis is triggered by a burst of ROS in mitochondria and via the activation of a RIP3-containing complex, but without any additional apoptosis inhibitors. In terms of activation, our glioblastoma model of necroptosis seems to be very relevant to what is observed in vivo following PDT but also following Ischemia/Reperfusion in the brain, heart and kidney [46].…”

Section: Discussionmentioning

confidence: 93%

RIP3 antagonizes a TSC2-mediated pro-survival pathway in glioblastoma cell death

Fettweis¹,

Valentin

L’homme³

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Glioblastomas are the deadliest type of brain cancer and are frequently associated with poor prognosis and a high degree of recurrence despite removal by surgical resection and treatment by chemo-and radio-therapy. Photodynamic therapy (PDT) is a treatment well known to induce mainly necrotic and apoptotic cell death in solid tumors. 5-Aminolevulinic acid (5-ALA)-based PDT was recently shown to sensitize human glioblastoma cells (LN-18) to a RIP3 (Receptor Interacting Protein 3)-dependent cell death which is counter-acted by activation of autophagy. These promising results led us to investigate the pathways involved in cell death and survival mechanisms occurring in glioblastoma following PDT. In the present study, we describe a new TSC2 (Tuberous Sclerosis 2)-dependent survival pathway implicating MK2 (MAPKAPK2) kinase and 14-3-3 proteins which conducts to the activation of a pro-survival autophagy. Moreover, we characterized a new RIP3/TSC2 complex where RIP3 is suggested to promote cell death by targeting TSC2-dependent survival pathway. These results highlight (i) a new role of TSC2 to protect glioblastoma against PDT-induced cell death and (ii) TSC2 and 14-3-3 as new RIP3 partners.

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Section: Discussionmentioning

confidence: 93%

RIP3 antagonizes a TSC2-mediated pro-survival pathway in glioblastoma cell death

Fettweis¹,

Valentin

L’homme³

et al. 2017

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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“…Phosphorylation of RIPK1 and RIPK3 has been recognized as another set of hallmarks for the activation of necroptosis (Jouan-Lanhouet et al, 2014). We characterized an antibody specifically recognizing phospho-S14/15 of human and mouse RIPK1 (Figure S2A–D).…”

Section: Resultsmentioning

confidence: 99%

Activation of Necroptosis in Multiple Sclerosis

et al. 2015

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Multiple sclerosis (MS), a common neurodegenerative disease of the CNS, is characterized by the loss of oligodendrocytes and demyelination. TNFα, a proinflammatory cytokine implicated in MS, can activate necroptosis, a necrotic cell death pathway regulated by RIPK1 and RIPK3 under caspase-8 deficient conditions. Here, we demonstrate defective caspase-8 activation, as well as, activation of RIPK1, RIPK3 and MLKL, the hallmark mediators of necroptosis, in the cortical lesions of human MS pathological samples. Furthermore, we show that MS pathological samples are characterized by an increased insoluble proteome in common with other neurodegenerative diseases such as AD, PD and HD. Finally, we show that necroptosis mediates oligodendrocyte degeneration induced by TNFα, and inhibition of RIPK1 protects against oligodendrocyte cell death in two animal models of MS and in culture. Our findings demonstrate that necroptosis is involved in MS and suggest that targeting RIPK1 may represent a novel therapeutic strategy for MS.

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“…Our results indicate that there is a discrepancy between both ␤-secretase and amyloid-␤ protein precursor, which was regulated down in the ischemic temporal cortex following 2 days after ischemia. It is clear now that this time necrotic neuronal cell death is associated with post-ischemic neuropathology [47,48]. During necrotic neuronal death, a loss of all cell membranes integrity was finally noted [49,50].…”

Section: Discussionmentioning

confidence: 96%

Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

Pluta

Kocki

Ułamek-Kozioł³

et al. 2016

JAD

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Abstract. Brain ischemia may be causally related with Alzheimer's disease. Presumably, ␤-secretase and amyloid-␤ protein precursor gene expression changes may be associated with Alzheimer's disease neuropathology. Consequently, we have examined quantitative changes in both ␤-secretase and amyloid-␤ protein precursor genes in the medial temporal lobe cortex with the use of quantitative rtPCR analysis following 10-min global brain ischemia in rats with survival of 2, 7, and 30 days. The greatest significant overexpression of ␤-secretase gene was noted on the 2nd day, while on days 7-30 the expression of this gene was only modestly downregulated. Amyloid-␤ protein precursor gene was downregulated on the 2nd day, but on days 7-30 postischemia, there was a significant reverse tendency. Thus, the demonstrated alterations indicate that the considerable changes of expression of ␤-secretase and amyloid-␤ protein precursor genes may be connected with a response of neurons in medial temporal lobe cortex to transient global brain ischemia. Finally, the ischemia-induced gene changes may play a key role in a late and slow onset of Alzheimer-type pathology.

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Necroptosis, in vivo detection in experimental disease models

Cited by 147 publications

References 167 publications

RIP3 antagonizes a TSC2-mediated pro-survival pathway in glioblastoma cell death

RIP3 antagonizes a TSC2-mediated pro-survival pathway in glioblastoma cell death

Activation of Necroptosis in Multiple Sclerosis

Discrepancy in Expression of β-Secretase and Amyloid-β Protein Precursor in Alzheimer-Related Genes in the Rat Medial Temporal Lobe Cortex Following Transient Global Brain Ischemia

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