TNF-α Triggers RIP1/FADD/Caspase-8-Mediated Apoptosis of Astrocytes and RIP3/MLKL-Mediated Necroptosis of Neurons Induced by Angiostrongylus cantonensis Infection

Zhou, Hongli; Zhou, Ming; Hu, Yue; Limpanon, Yanin; Ma, Yu-Bin; Huang, Ping; Dekumyoy, Paron; Maleewong, Wanchai; Lv, Ziquan

doi:10.1007/s10571-021-01063-w

Cited by 24 publications

(17 citation statements)

References 60 publications

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“…It possesses activities that are both kinase dependent and kinase independent [ 41 ]. RIPK1 can form a complex with FADD and caspase-8, in line with a previously reported signaling axis that interacts with FADD and caspase-8 to increase cell death [ 43 , 44 ]. The amino acid Asp325 of RIPK1 is required for avoiding aberrant cell death in response to TNF, indicating that caspase-8 cleavage of RIPK1 is a method of disassembling death-inducing complexes [ 44 ].…”

Section: Comparison Of Proteins In Both Apoptosis and Necroptosis Pathwayssupporting

confidence: 83%

Differences of Key Proteins between Apoptosis and Necroptosis

Park

Vetrivel

et al. 2021

BioMed Research International

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Many different types of programmed cell death (PCD) have been identified, including apoptosis and necroptosis. Apoptosis is a type of cell death that is controlled by various genes. It is in charge of eliminating aberrant cells such as cancer cells, replenishing normal cells, and molding the body as it develops. Necroptosis is a type of programmed cell death that combines necrosis and apoptosis. In other words, it takes on a necrotic appearance, although cells die in a controlled manner. Various investigations of these two pathways have revealed that caspase-8, receptor-interacting serine/threonine-protein kinase 1 (RIPK1), and RIPK3 are crucial proteins in charge of the switching between these two pathways, resulting in the activation or inhibition of necroptosis. In this review, we have summarized the key proteins between apoptosis and necroptosis.

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Section: Comparison Of Proteins In Both Apoptosis and Necroptosis Pathwayssupporting

confidence: 83%

Differences of Key Proteins between Apoptosis and Necroptosis

Park

Vetrivel

et al. 2021

BioMed Research International

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“…Circulating TNF-a is able to migrate into the brain via endothelial cells expressing TNF-a receptors 1 and 2 (TNFR1 and TNFR2) in the BBB (76,77). Once in the brain and upon binding to receptors on glial cells, TNF-a can augment the inflammatory signals by activating astrocytes and microglia, which lead to the local production of TNF-a in the brain (78,79). Binding of TNF-a to TNFR recruits intracellular proteins and transduces inflammatory signaling, leading to NF-kB translocating to the nucleus (80,93).…”

Section: Inflammationmentioning

confidence: 99%

Doxorubicin-Induced Cognitive Impairment: The Mechanistic Insights

Zhang

et al. 2021

Front. Oncol.

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Chemotherapy can significantly prolong the survival of patients with breast cancer; Nevertheless, the majority of patients receiving chemotherapy such as doxorubicin may have cognitive deficits that manifest as impairments in learning, reasoning, attention, and memory. The phenomenon of chemotherapy-induced cognitive decline is termed as chemotherapy-related cognitive impairment (CRCI) or chemo-brain. Doxorubicin (DOX), a commonly used drug in adjuvant chemotherapy for patients with breast cancer, has been reported to induce chemo-brain through a variety of mechanisms including DNA damage, oxidative stress, inflammation, dysregulation of apoptosis and autophagy, changes in neurotransmitter levels, mitochondrial dysfunction, glial cell interactions, neurogenesis inhibition, and epigenetic factors. These mechanisms do not operate independently but are inter-related, coordinately contributing to the development of chemo-brain. Here we review the relationships of these mechanisms and pathways in attempt to provide mechanistic insights into the doxorubicin-induced cognitive impairment.

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“…Third-stage larvae of AC (AC L3) were obtained from positive Biomphalaria glabrata ( B . glabrata ), as described previously [ 26 ]. Briefly, B .…”

Section: Methodsmentioning

confidence: 99%

Stat3/IL-6 signaling mediates sustained pneumonia induced by Agiostrongylus cantonensis

Zhou

Wei

et al. 2022

PLoS Negl Trop Dis

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Angiostrongylus cantonensis (AC) is well-documented that parasitizes the host brain and causes eosinophilic meningitis. The migration route of AC in permissive hosts is well demonstrated, while in nonpermissive hosts, it remains to be fully defined. In the present study, we exploited live imaging technology, morphological and pathological configuration analysis, and molecular biological technologies to explore the migration route of AC and the accompanying tissue damage in nonpermissive and permissive hosts. Our data indicated that, in nonpermissive host mouse, AC larvae migrated from intestinal wall to liver at 2 hours post-infection (hpi), from liver to lung at 4 hpi and then from lung to brain at 8 hpi. AC larval migration caused fatal lung injury (pneumonia) during acute and early infection phases, along with significant activation of Stat3/IL-6 signaling. In addition, AC induce sustained interstitial pneumonia in mouse and rat and pulmonary fibrosis only in rat during late infection phase. Moreover, during the early and late infection phases, Th2 cytokine expression and Stat3 and IL-6 signaling were persistently enhanced and myeloid macrophage cells were notably enriched in host lung, and administration of Stat3 and IL-6 inhibitors (C188-9 and LMT-28) attenuated AC infection-induced acute pneumonia in mice. Overall, we are the first to provide direct and systemic laboratory evidence of AC migration route in a nonpermissive host and report that infection with a high dose of AC larvae could result in acute and fatal pneumonia through Stat3/IL-6 signaling in mice. These findings may present a feasible to rational strategy to minimize the pathogenesis induced by AC.

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TNF-α Triggers RIP1/FADD/Caspase-8-Mediated Apoptosis of Astrocytes and RIP3/MLKL-Mediated Necroptosis of Neurons Induced by Angiostrongylus cantonensis Infection

Cited by 24 publications

References 60 publications

Differences of Key Proteins between Apoptosis and Necroptosis

Differences of Key Proteins between Apoptosis and Necroptosis

Doxorubicin-Induced Cognitive Impairment: The Mechanistic Insights

Stat3/IL-6 signaling mediates sustained pneumonia induced by Agiostrongylus cantonensis

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