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 (TAS) 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. J. Cell. Biochem. 115: 2116-2122, 2014.

Sirangelo, I., Giovane, A., Maritato, R., D'Onofrio, N., Iannuzzi, C., Giordano, A., et al. (2014). Platelet-activating factor mediates the cytotoxicity induced by w7fw14f apomyoglobin amyloid aggregates in neuroblastoma cells. JOURNAL OF CELLULAR BIOCHEMISTRY, 115(12), 2116-2122 [10.1002/jcb.24888].

Platelet-activating factor mediates the cytotoxicity induced by w7fw14f apomyoglobin amyloid aggregates in neuroblastoma cells

Giordano A.;
2014-01-01

Abstract

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 (TAS) 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. J. Cell. Biochem. 115: 2116-2122, 2014.
2014
Sirangelo, I., Giovane, A., Maritato, R., D'Onofrio, N., Iannuzzi, C., Giordano, A., et al. (2014). Platelet-activating factor mediates the cytotoxicity induced by w7fw14f apomyoglobin amyloid aggregates in neuroblastoma cells. JOURNAL OF CELLULAR BIOCHEMISTRY, 115(12), 2116-2122 [10.1002/jcb.24888].
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11365/1129667
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