The role of tumor necrosis factor receptor superfamily members in mammalian brain development, function and homeostasis

Twohig, Jason Peter; Cuff, Simone; Yong, Audrey Alice; Wang, Edward Chung Yern

doi:10.1515/rns.2011.041

Cited by 26 publications

(24 citation statements)

References 273 publications

(450 reference statements)

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“…TL1A and DR3 generally are known for low basal expression with most research focused on lymphocytes and autoimmune diseases [42], although previous studies have identified TL1A mRNA in mouse brain [28]. A characteristic of TNF receptor signaling is amplification of ligands, receptors, and cascade signaling components within and across cells; in brain this likely involves glia and neurons [3,24]. We found TRADD, FADD, and pFADD expression increased about fourfold, consistent with amplification of TL1A, DR3, and FasL initiating TL1A-DR3-TRADD-FADD-procaspase 8 complexes referred to as DISC ((DISC,27)).…”

Section: Discussionmentioning

confidence: 99%

“…DRs initiate a death-inducing signaling complex (DISC) of proteins that share DDs leading to CC3-induced cell death through multiple paths. The DD-containing receptors death receptor 3 (DR3, TNFRSF25) and Fas receptor (Fas, FasR, CD95, TNFRSF6) are expressed at low levels in the hippocampus of rodents and humans [24]. The TNFSF agonists TNF-like 1A (TL1A, TNFSF15, VEGI) for DR3 and Fas ligand (FasL, TNFSF6, CD95L) for FasR, are also expressed in brain, as are components of the DISC, i.e., the DDsignaling protein Fas-associated death domain (FADD) and caspase-8, an initiator caspase.…”

Section: Introductionmentioning

confidence: 99%

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Hippocampal TNF-death receptors, caspase cell death cascades, and IL-8 in alcohol use disorder

Vetreno

Crews

2020

Mol Psychiatry

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The relationship between increased neuroimmune gene expression and hippocampal degeneration in alcohol use disorder (AUD) and other mental diseases is poorly understood. We report here that tumor necrosis factor receptor superfamily death receptor 3 (TNFRSF25, DR3) and Fas receptors (Fas) that initiate caspase cell death cascades are increased in AUD hippocampus and following a rat adolescent binge drinking model. Death receptors are known inducers of apoptosis and cell death that recruit death domain (DD) proteins FADD and TRADD and caspases to form death-inducing signaling complexes (DISC). In postmortem human AUD hippocampus, mRNA and IHC protein are increased for the entire death receptor cascade. In AUD hippocampus, ligand-death receptor pairs, i.e., TL1A-DR3 and FasL-Fas, were increased, as well as FADD and TRADD, and active caspase-8,-7,-9, and caspase-3. Further, pNFκB p65, a key neuroimmune transcription factor, and IL-8, a chemokine, were significantly increased. Interestingly, across AUD patients, increases in DR3 and Fas correlated with TRADD, and TRADD with active caspase+IR and IL-8+IR, consistent with coordinated activation of neuronal DISC mediated death cascades and neuroimmune gene induction in AUD. These findings support a role for DR3 and Fas neuroimmune signaling in AUD hippocampal neurodegeneration.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Hippocampal TNF-death receptors, caspase cell death cascades, and IL-8 in alcohol use disorder

Vetreno

Crews

2020

Mol Psychiatry

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“…It is likely that multiple mechanisms regulate the effects of cytokines on offspring brain development, with specific mechanisms depending on timing of exposure. These include: dysregulation of nerve growth factors (Schobitz et al 1993; Anisman & Merali, 2002; Gilmore et al 2003; Twohig et al 2011); loss of dendritic connections (Marx et al 2001; Gilmore et al 2004; Twohig et al 2011) and white matter connectivity (Yoon et al 1996; Dammann & Leviton, 1997); apoptosis (Hu et al 1997); dysregulation of neurotransmitters (Zalcman et al 1994; Behrens et al 2008); and hormonal dysregulation (Schobitz et al 1993; Anisman & Merali, 2002) impeding healthy sexual differentiation of the brain (Handa et al 1994; Kawata, 1995; Tobet & Hanna, 1997; Goldstein et al 2001; Tobet, 2002) and brain aging (Zietz et al 2001). …”

Section: Discussionmentioning

confidence: 99%

Prenatal maternal immune disruption and sex-dependent risk for psychoses

et al. 2014

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Background Previous studies suggest that abnormalities in maternal immune activity during pregnancy alter the offspring’s brain development and are associated with increased risk for schizophrenia (SCZ) dependent on sex. Method Using a nested case–control design and prospectively collected prenatal maternal sera from which interleukin (IL)-1β, IL-8, IL-6, tumor necrosis factor (TNF)-α and IL-10 were assayed, we investigated sex-dependent associations between these cytokines and 88 psychotic cases [SCZ=44; affective psychoses (AP)=44] and 100 healthy controls from a pregnancy cohort followed for >40 years. Analyses included sex-stratified non-parametric tests adjusted for multiple comparisons to screen cytokines associated with SCZ risk, followed by deviant subgroup analyses using generalized estimating equation (GEE) models. Results There were higher prenatal IL-6 levels among male SCZ than male controls, and lower TNF-α levels among female SCZ than female controls. The results were supported by deviant subgroup analyses with significantly more SCZ males with high IL-6 levels (>highest quartile) compared with controls [odd ratio (OR)75=3.33, 95% confidence interval (CI) 1.13–9.82], and greater prevalence of low TNF-α levels (

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“…Of particular relevance to the developing brain, it has recently been demonstrated that microglia play a crucial role in normal postnatal synaptic pruning via complement signaling (Schafer et al, 2012). Further, members of the tumor necrosis factor receptor super family have been implicated in the regulation of neuronal progenitor proliferation, differentiation and patterning (Saliba and Henrot, 2001; Twohig et al, 2011). These findings highlight the complex interplay between the CNS and immune response, which is likely to influence both normal brain development as well as the brain's response to injury (Bilbo and Schwarz, 2012).…”

Section: Innate and Adaptive Immunitymentioning

confidence: 99%

Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across species

Semple

Blomgren

Gimlin

et al. 2013

Progress in Neurobiology

1,640

1,372

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Hypoxic-ischemic and traumatic brain injuries are leading causes of long-term mortality and disability in infants and children. Although several preclinical models using rodents of different ages have been developed, species differences in the timing of key brain maturation events can render comparisons of vulnerability and regenerative capacities difficult to interpret. Traditional models of developmental brain injury have utilized rodents at postnatal day 7–10 as being roughly equivalent to a term human infant, based historically on the measurement of post-mortem brain weights during the 1970s. Here we will examine fundamental brain development processes that occur in both rodents and humans, to delineate a comparable time course of postnatal brain development across species. We consider the timing of neurogenesis, synaptogenesis, gliogenesis, oligodendrocyte maturation and age-dependent behaviors that coincide with developmentally regulated molecular and biochemical changes. In general, while the time scale is considerably different, the sequence of key events in brain maturation is largely consistent between humans and rodents. Further, there are distinct parallels in regional vulnerability as well as functional consequences in response to brain injuries. With a focus on developmental hypoxicischemic encephalopathy and traumatic brain injury, this review offers guidelines for researchers when considering the most appropriate rodent age for the developmental stage or process of interest to approximate human brain development.

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The role of tumor necrosis factor receptor superfamily members in mammalian brain development, function and homeostasis

Cited by 26 publications

References 273 publications

Hippocampal TNF-death receptors, caspase cell death cascades, and IL-8 in alcohol use disorder

Hippocampal TNF-death receptors, caspase cell death cascades, and IL-8 in alcohol use disorder

Prenatal maternal immune disruption and sex-dependent risk for psychoses

Brain development in rodents and humans: Identifying benchmarks of maturation and vulnerability to injury across species

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