Metabolism and Functions of Platelet-Activating Factor (PAF) in the Nervous Tissue

Goracci, G; Balestrieri, Maria Luisa; Nardicchi, Vincenza

doi:10.1007/978-0-387-30378-9_13

Cited by 9 publications

(17 citation statements)

References 338 publications

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“…In addition, cross-talks also exist between the pathways regulating their expression and activity [64]. It is likely that both cPLA 2 and sPLA 2 are also involved in the biosynthesis of PAF by the remodeling pathway producing 1-alkyl-2-lyso-sn-glycero-3-phosphocholine from membrane 1-alkyl-2-acyl-sn-glycero-3-phosphocholine in neural cells [65,66].…”

Section: Production Of Lipid Mediatorsmentioning

confidence: 97%

Low Molecular Weight Phospholipases A2 in Mammalian Brain and Neural Cells: Roles in Functions and Dysfunctions

2010

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Several "low molecular weight" or "secretory" phospholipases A(2) isoforms may be expressed in mammalian neural cells. Indeed, mRNAs for GIB, GIIA, GIIE, GIII, GV, GX, and GXII were detected in brain tissues despite different levels. However, only the presence of GIB, GIIA, and GV proteins has been clearly demonstrated in neural cells or in the nervous tissue. Although the roles of GIB and GV in the nervous tissue are still elusive, there is evidence to support the involvement of GIIA in physiological and pathological events, including neurotransmission, long-term potentiation, and neuritogenesis. The neurotoxic effects of an increase in GIIA may be envisaged under pathological conditions associated with the activation of astrocytes during inflammation or through activation of neurons and enzymes due to the stimulation of the NMDA glutamate receptor. In the past, elevation of GIIA expression in many acute and chronic neurological diseases is well known. Although each neurodegenerative disease has a separate etiology, many share similar neurochemical common processes, such as excitotoxicity, oxidative stress, and mitochondrial dysfunction, phenomena where GIIA play an important role.

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Section: Production Of Lipid Mediatorsmentioning

confidence: 97%

Low Molecular Weight Phospholipases A2 in Mammalian Brain and Neural Cells: Roles in Functions and Dysfunctions

2010

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“…Increased levels of PAF, due to upregulation of biosynthetic pathways or to downregulation of its degradation through the PAF–AH, are reported in neuroinflammation, brain ischemia, and neurodegenerative diseases [Goracci et al, ]. Therefore, we next evaluated the time‐dependent effect of W7FW14F ApoMb on the PAF–AH II expression levels (from time 0 up to 60 min).…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, neurons pre‐treated with PAF receptor (PAF‐R) antagonists were resistant to Aβ1–42 [Bate et al, ,, , ; Li et al, ]. On the other hand, increased levels of PAF due to downregulation of its degradation catalyzed by the PAF‐acetylhydrolase (AH) type I (PAF–AH I) or II (PAF–AH II) are critically involved in neurodegenerative diseases [Goracci et al, ]. In particular, the PAF–AH II contains three separate catalytic activities, namely acetylhydrolase (AH), lysophospholipid transacetylase (TA L ), and sphingosine transacetylase (TA S ), through which PAF functions are modified by hydrolyzing PAF to lyso‐PAF (AH) or converting PAF to acyl analogs of PAF (TA L ) or N‐acetylsphingosine (TA S ) [Balestrieri et al, ].…”

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confidence: 99%

Platelet‐Activating Factor Mediates the Cytotoxicity Induced by W7FW14F Apomyoglobin Amyloid Aggregates in Neuroblastoma Cells

Sirangelo

Giovane

Maritato

et al. 2014

J of Cellular Biochemistry

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W7FW14F apomyoglobin (W7FW14F ApoMb) amyloid aggregates induce cytotoxicity in SH-SY5Y human neuroblastoma cells through a mechanism not fully elucidated. Amyloid neurotoxicity process involves calcium dyshomeostasis and reactive oxygen species (ROS) production. Another key mediator of the amyloid neurotoxicity is Platelet-Activating Factor (PAF), an inflammatory phospholipid implicated in neurodegenerative diseases. Here, with the aim at evaluating the possible involvement of PAF signaling in the W7FW14F ApoMb-induced cytotoxicity, we show that the presence of CV3899, a PAF receptor (PAF-R) antagonist, prevented the detrimental effect of W7FW14F ApoMb aggregates on SH-SY5Y cell viability. Noticeably, we found that the activation of PAF signaling, following treatment with W7FW14F ApoMb, involves a decreased expression of the PAF acetylhydroase II (PAF-AH II). Interestingly, the reduced PAF-AH II expression was associated with a decreased acetylhydrolase (AH) activity and to an increased sphingosine-transacetylase activity (TA(S)) with production of N-acetylsphingosine (C2-ceramide), a well known mediator of neuronal caspase-dependent apoptosis. These findings suggest that an altered PAF catabolism takes part to the molecular events leading to W7FW14F ApoMb amyloid aggregates-induced cell death.

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“…PAF, a potent inflammatory lipid, plays crucial roles in the neuronal damage and death in various pathological conditions (Prescott et al, 2000; Tong et al, 2001; Bate et al, 2004a; Xu and Tao, 2004; Bazan, 2005; Goracci et al, 2009; Balestrieri et al, 2010; Farooqui et al, 2010). The detrimental effects of the excessive accumulation of PAF in the brain are also supported by the neuroprotection exerted by PAF receptor antagonists (Brewer et al, 2002; Shi et al, 2010).…”

Section: Paf‐induced Neuronal Toxicitymentioning

confidence: 99%

“…The detrimental effects of the excessive accumulation of PAF in the brain are also supported by the neuroprotection exerted by PAF receptor antagonists (Brewer et al, 2002; Shi et al, 2010). The PAF‐induced neuronal toxicity is mainly characterized by increased levels of PAF due to up‐regulation of PAF biosynthetic pathways or downregulation of PAF catabolic pathway (Goracci et al, 2009).…”

Section: Paf‐induced Neuronal Toxicitymentioning

confidence: 99%

Amyloid toxicity and platelet‐activating factor signaling

Sirangelo¹,

Irace²,

Balestrieri³

2013

Journal Cellular Physiology

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Amyloidosis is the accumulation of insoluble proteinaceous aggregates in vivo and is implicated in many neurodegenerative diseases, including Alzheimer's, Huntington's, and Parkinson's diseases. This article briefly reviews the current knowledge of amyloid aggregate toxicity and inflammatory signaling in the nervous system. In particular, we focus our attention on the role of platelet-activating factor (PAF) as mediator of amyloid cytotoxicity.

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Metabolism and Functions of Platelet-Activating Factor (PAF) in the Nervous Tissue

Cited by 9 publications

References 338 publications

Low Molecular Weight Phospholipases A2 in Mammalian Brain and Neural Cells: Roles in Functions and Dysfunctions

Low Molecular Weight Phospholipases A2 in Mammalian Brain and Neural Cells: Roles in Functions and Dysfunctions

Platelet‐Activating Factor Mediates the Cytotoxicity Induced by W7FW14F Apomyoglobin Amyloid Aggregates in Neuroblastoma Cells

Amyloid toxicity and platelet‐activating factor signaling

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