Particulate matter (PM2.5) exposure season-dependently induces neuronal apoptosis and synaptic injuries

Chen, Minjun; Li, Ben; Sang, Nan

doi:10.1016/j.jes.2016.10.013

Cited by 47 publications

(23 citation statements)

References 33 publications

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“…Kulas et al () found that prenatal exposure to PM2.5 in mice led to elevated SYP expression and unchanged PSD95 expression in the hippocampus of male offspring. Zhang et al () reported that prenatal PM2.5 exposure in mice decreased postsynaptic densities of membranes and the number of synaptic vesicles in the cerebral cortex of offspring, and an in vitro study suggested that PM2.5 exposure reduced PSD95 expression in cortical neurons (Chen, Li, & Sang, ). These results suggested that PM2.5 exposure during early life might change synaptic structural plasticity.…”

Section: Discussionmentioning

confidence: 99%

Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

Liu

Yang

et al. 2019

Brain and Behavior

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IntroductionFine particulate matter (PM2.5) is closely associated with many neurological disorders including neurodegenerative disease, stroke, and brain tumors. However, the toxic effects of PM2.5 on neurodevelopment remain unclear. In this study, we aimed to determine the neurotoxic effects of early postnatal exposure to PM2.5 in immature and mature rats.MethodsWe exposed neonatal rats to PM2.5 (2 or 10 mg/kg body weight) through intranasal instillation from postnatal day (PND) 3–15, once a day. Emotional and cognitive development were evaluated using the elevated plus maze, forced swimming, and Morris water maze tests. Hippocampal tissue was collected and subjected to transmission electron microscopy observation and western blot analysis.ResultsRats had lower body weight after exposure to high dose of PM2.5. The behavioral test results indicated that high‐dose PM2.5 exposure led to increased anxiety‐like symptoms in immature and mature rats, apparent depressive‐like behaviors in mature rats, and impaired spatial learning and memory abilities in immature rats, and low‐dose PM2.5 exposure increased anxiety‐like behaviors in immature rats. Further, high‐dose PM2.5 exposure contributed to fewer synapses, thinner postsynaptic density, and shorter active zone in immature and mature rats, and also decreased expressions of synaptophysin (SYP), growth associated protein‐43 (GAP43), and postsynaptic density‐95 (PSD95) in immature rats, SYP and PSD95 in mature rats. Moreover, low‐dose PM2.5 exposure diminished the expression of PSD95 in immature rats. In addition, high‐dose PM2.5 exposure reduced brain‐derived neurotrophic factor (BDNF) expression and cAMP response element binding protein (CREB) phosphorylation in both immature and mature rats, and low‐dose PM2.5 exposure lessened BDNF expression and CREB phosphorylation in immature rats.ConclusionsOur findings indicate that PM2.5 impairs emotional and cognitive development by disrupting structural synaptic plasticity, possibly via the CREB/BDNF signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

Liu

Yang

et al. 2019

Brain and Behavior

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“…The PM 2.5 sampling point was located in Taiyuan (112°21–34′E longitude, 37°47–48′N latitude) of Shanxi Province. The samples were collected onto quartz filters (Φ90 mm, Munktell, Falun, Dalarna, Sweden) with PM middle-volume air samplers (TH-150CIII, Wuhan, China) from November 2012 to February 2013 according to our previously reported conditions [ 84 ], and the PM characterization was presented in our recently published work (Additional file 1 : Table S1) [ 85 ]. The collected PM 2.5 was transferred into aqueous suspension by soaking the PM 2.5 -loaded filters in Milli-Q deionized water for 30 min, followed by vortexing (5 min) and sonication (30 min).…”

Section: Methodsmentioning

confidence: 99%

NF-κB-regulated microRNA-574-5p underlies synaptic and cognitive impairment in response to atmospheric PM2.5 aspiration

Gao

et al. 2017

Part Fibre Toxicol

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BackgroundPM2.5 (particulate matter ≤ 2.5 μm) is one of the leading environmental risk factors for the global burden of disease. Whereas increasing evidence has linked the adverse roles of PM2.5 with cardiovascular and respiratory diseases, limited but growing emerging evidence suggests that PM2.5 exposure can affect the nervous system, causing neuroinflammation, synaptic dysfunction and cognitive deterioration. However, the molecular mechanisms underlying the synaptic and cognitive deficits elicited by PM2.5 exposure are largely unknown.MethodsC57BL/6 mice received oropharyngeal aspiration of PM2.5 (1 and 5 mg/kg bw) every other day for 4 weeks. The mice were also stereotaxically injected with β-site amyloid precursor protein cleaving enzyme 1 (β-secretase, BACE1) shRNA or LV-miR-574-5p lentiviral constructs in the absence or presence of PM2.5 aspiration at 5 mg/kg bw every other day for 4 weeks. Spatial learning and memory were assessed with the Morris water maze test, and synaptic function integrity was evaluated with electrophysiological recordings of long-term potentiation (LTP) and immunoblot analyses of glutamate receptor subunit expression. The expression of α-secretase (ADAM10), BACE1, and γ-secretase (nicastrin) and the synthesis and accumulation of amyloid β (Aβ) were measured by immunoblot and enzyme-linked immunosorbent assay (ELISA). MicroRNA (miRNA) expression was screened with a microRNA microarray analysis and confirmed by real-time quantitative reverse transcription PCR (qRT-PCR) analysis. Dual-luciferase reporter gene and chromatin immunoprecipitation (ChIP) analyses were used to detect the binding of miR-574-5p in the 3’UTR of BACE1 and NF-κB p65 in the promoter of miR-574-5p, respectively.ResultsPM2.5 aspiration caused neuroinflammation and deteriorated synaptic function integrity and spatial learning and memory, and the effects were associated with the induction of BACE1. The action was mediated by NF-κB p65-regulated downregulation of miR-574-5p, which targets BACE1. Overexpression of miR-574-5p in the hippocampal region decreased BACE1 expression, restored synaptic function, and improved spatial memory and learning following PM2.5 exposure.ConclusionsTaken together, our findings reveal a novel molecular mechanism underlying impaired synaptic and cognitive function following exposure to PM2.5, suggesting that miR-574-5p is a potential intervention target for the prevention and treatment of PM2.5-induced neurological disorders.Electronic supplementary materialThe online version of this article (10.1186/s12989-017-0215-3) contains supplementary material, which is available to authorized users.

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“…Concerning to about PM 2.5 exposure induced neuronal apoptosis, evidence from mouse model of gestational PM 2.5 exposure showed neuronal apoptosis in hippocampus of mice offspring [24]. In vitro data also showed that PM 2.5 exposure season-dependently induced neuronal apoptosis and synaptic injuries [9]. From our results, TUNEL positive cells were obviously increased in CA1 area of the hippocampus from mice exposed to PM 2.5 for 24 weeks, indicating elevated neuronal apoptosis rate by PM 2.5 exposure ( Fig.…”

Section: Discussionmentioning

confidence: 95%

“…PC12 cells were cultured in DMEM (BBI Life Sciences, China) supplemented with 10% fetal bovine serum (FBS) (Thermo Fisher Scienti c, USA), 1% penicillin-streptomycin (BBI Life Sciences, China), and maintained in an incubator at 37 °C with 5% CO 2 . Primary hippocampal neurons were prepared from the brains of C57BL/6 at postnatal day 1 as previously described [43] and brie y described in supplementary materials.…”

Section: Brain Slice Preparation and Tunel Testmentioning

confidence: 99%

“…Neuronal apoptosis is considered a crucial event in the development of neurodegenerative diseases, which is closely related to the pathologic degree of such diseases [8]. Additionally, Chen found that PM 2.5 exposure could induce neuronal apoptosis and synaptic injuries in a season-dependent manner, accompanied by changes in apoptosis-related proteins in vitro [9], although little was known about the mechanism by which PM 2.5 triggered apoptosis. Therefore, we speculate that neuronal apoptosis may be critical event in the pathogenesis of cognitive dysfunction induced by PM 2.5 exposure in mice.…”

Section: Introductionmentioning

confidence: 99%

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S-adenosylmethionine Decarboxylase 1 Participates in PM2.5 Exposure Induced Neuronal Apoptosis via Mitochondria-Mediated Pathway

Zhu

Shou

et al. 2020

Preprint

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Background: Fine particle (Particulate matter 2.5, PM2.5), as the primary ambient pollutant, is considered harmful to some neurodegenerative diseases, while the specific biochemical mechanism underlying is still unrevealed. Neuronal apoptosis is believed the crucial event in neurodegenerative pathogenesis, but evidence supporting neuronal apoptosis as PM2.5 induced neuronal injury is insufficient. S-adenosylmethionine decarboxylase 1 (AMD1) and its related spermidine synthesis have been shown to participate in cellular apoptosis, but its role in PM2.5 exposure induced neuronal apoptosis was rarely reported. To better understand contribution of AMD1 activity and spermidine in PM2.5 exposure induced neuronal apoptosis, may provide novel therapeutic and preventive targets for air pollution associated neurodegenerative diseases.Methods: In the current work, sixteen C57BL/6 male mice were randomly divided into ambient PM2.5 chamber or filtered air chamber, and the mouse model of whole-body ambient PM2.5 chronic exposure was established. Behavioral and cognitive ability, together with corresponding biomedical index were recorded and tested to evaluated neurotoxicity by PM2.5 exposure in mice. In parallel, PC12 cells and primary hippocampal neurons were applied for PM2.5 treatment to explore the possible cellular and molecular mechanism which may be critically involved in the process. AMD1 activity and cellular spermidine content were modulated by pharmacological approach to examine their participation in PM2.5 triggered neuronal apoptosis, followed by better examination of typical index for mitochondrial membrane potential and mitochondrial-mediated apoptosis pathway signaling.Results: Chronic ambient PM2.5 exposure attenuated spatial learning and memory ability, and triggered neuronal apoptosis together with increased expression of apoptosis-related Bax/Bcl-2 and cleaved caspase-3. PM2.5 exposure impaired AMD1 expression and spermidine synthesis. AMD1 inhibition could mimick PM2.5 exposure induced neuronal apoptosis. Spermidine supplementation rescued against neurotoxicity and inhibited PM2.5 induced apoptosis, in which mitochondrial pathway signaling.Conclusions: Chronic real-time exposure to ambient PM2.5 led to the reduced the ability of spatial learning and memory in mice. Neuronal apoptosis was the key event in the process of neurodegenerative development induced by PM2.5 exposure. AMD1 and spermidine participated in neuronal apoptosis induced by PM2.5 exposure, which was at least partially dependent on mitochondria mediated pathway.

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Particulate matter (PM2.5) exposure season-dependently induces neuronal apoptosis and synaptic injuries

Cited by 47 publications

References 33 publications

Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

Effects of early postnatal exposure to fine particulate matter on emotional and cognitive development and structural synaptic plasticity in immature and mature rats

NF-κB-regulated microRNA-574-5p underlies synaptic and cognitive impairment in response to atmospheric PM2.5 aspiration

S-adenosylmethionine Decarboxylase 1 Participates in PM2.5 Exposure Induced Neuronal Apoptosis via Mitochondria-Mediated Pathway

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