Neuroprotective Peptide NAPVSIPQ Antagonizes Ethanol Inhibition of L1 Adhesion by Promoting the Dissociation of L1 and Ankyrin-G

Dou, Xiaowei; Lee, Jerry Y.; Charness, Michael E.

doi:10.1016/j.biopsych.2019.08.020

Cited by 9 publications

(6 citation statements)

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“…31 For instance, Dou et al suggested that EphB2 plays a critical role in synaptic development, and its potent activation by NAP suggests that ADNP may mediate synaptic development partly by activating EphB2. 34 Zhang et al demonstrated that EphB2 was a critical factor that contributes to the vulnerability to stress and might be a potential target for the treatment of depression. 35 Additionally, a recent study validated that age-associated increase in miR-204 level and age-related loss of EphB2 might contribute to cognitive deficits by accelerating this deterioration.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of miR-204-5p downregulation against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation

Liu

Wang

et al. 2021

Hum Exp Toxicol

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Background: Isoflurane, one of the most commonly used inhalational anesthetics, is usually used in surgery patients and often causes long-term learning and memory impairment. The aim of this study was to explore the role of microRNA-204-5p (miR-204-5p) in isoflurane-induced learning and memory impairment in rats. Methods: The Morris Water Maze (MWM) test was used to estimate the spatial learning and memory abilities of laboratory rats. Enzyme-linked immunosorbent assay (ELISA) was used to determine interleukin-6 (IL-6), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) concentrations in the hippocampal tissues. The expression level of miR-204-5p was determined by using quantitative reverse transcription polymerase chain reaction (qRT-PCR). The potential target genes of miR-204-5p were predicted and verified by the TargetScan and dual-luciferase reporter assay, respectively. Results: Isoflurane-induced rats showed significantly higher neurological function scores, higher escape latency and shorter time spent in the original quadrant. Isoflurane could significantly induce neuroinflammation, and the expression of miR-204-5p was increased in the hippocampal tissue of rats exposed to isoflurane. Moreover, downregulation of miR-204-5p attenuated the effect of isoflurane treatment on the escape latency and the time in the original quadrant, and inflammatory cytokines level was downregulated by inhibiting the expression of miR-204-5p. EphB2 was verified as a direct target gene of miR-204-5p. Conclusion: Downregulated miR-204-5p exerts protective effects against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation. MiR-204-5p could serve as a potential therapeutic target for the lightening of cognitive dysfunction induced by isoflurane.

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Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of miR-204-5p downregulation against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation

Liu

Wang

et al. 2021

Hum Exp Toxicol

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“…Several developmentally important molecular targets of alcohol, including the L1 neural cell adhesion molecule and GABA A receptors, are disrupted at blood alcohol concentrations attained after one or two US standard drinks [62][63][64][65][66] . Hence, repeated exposure to low levels of alcohol or a single exposure at critical periods in gestation could affect development.…”

Section: Mechanisms/pathophysiologymentioning

confidence: 99%

“…137 ). The sensitivity of L1 to alcohol is regulated by phosphorylation, which promotes L1 association with the cytoskeleton 62,138 . Importantly, molecules that block alcohol inhibition of L1 adhesion prevent the teratogenic effects of alcohol in mouse embryos 62,139 .…”

Section: Primermentioning

confidence: 99%

Fetal alcohol spectrum disorders

Popova

Charness

Burd

et al. 2023

Nat Rev Dis Primers

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117

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Alcohol readily crosses the placenta and may disrupt fetal development. Harm from prenatal alcohol exposure (PAE) is determined by the dose, pattern, timing and duration of exposure, fetal and maternal genetics, maternal nutrition, concurrent substance use, and epigenetic responses. A safe dose of alcohol use during pregnancy has not been established. PAE can cause fetal alcohol spectrum disorders (FASD), which are characterized by neurodevelopmental impairment with or without facial dysmorphology, congenital anomalies and poor growth. FASD are a leading preventable cause of birth defects and developmental disability. The prevalence of FASD in 76 countries is >1% and is high in individuals living in out-of-home care or engaged in justice and mental health systems. The social and economic effects of FASD are profound, but the diagnosis is often missed or delayed and receives little public recognition. Future research should be informed Nature Reviews Disease Primers | (2023) 9:11 2 0123456789();: PrimerFASD occur in all socioeconomic and ethnic groups 15 and are complex, chronic conditions that affect health and family functioning 16 . Individuals with FASD usually require lifelong health care as well as social and vocational support. Some require remedial education and others interact with the justice system. Early diagnosis and a strength-based management approach will optimize health outcomes.FASD are the most common of the potentially preventable conditions associated with birth anomalies and neurodevelopmental problems 13 , and their global effects, including huge social and economic costs, are substantial 17 . For example, in Canada, the annual cost associated with FASD is an estimated ~CAD$ 1.8 billion (CAD$ 1.3 billion to CAD$ 2.3 billion) 17 , which is attributable in part to productivity loss (41%), correction services (29%) and health care (10%). In North America, the lifetime cost of supporting an individual with FASD is estimated at >CAD$ 1 million 18 . Addressing and preventing alcohol use in pregnancy is a public-health imperative.This Primer presents the epidemiology of FASD and the latest understanding of its pathophysiology as well as approaches to diagnosis, screening and prevention. The Primer also describes outcomes across the lifespan, management and quality of life (QOL) of people living with FASD, and highlights important areas for future research and clinical practice. Epidemiology Alcohol use during pregnancyNo safe level of PAE has been established 19 , and international guidelines advise against any amount or type of alcohol use during pregnancy [20][21][22][23] . Nevertheless, ~10% of pregnant women worldwide consume alcohol 24,25 . The highest prevalence of alcohol use during pregnancy is in the WHO European Region (25.2% 24 ; Fig. 1), consistent with the prevalence of heavy alcohol use, heavy episodic drinking and alcohol use disorders in this region 26 . 0123456789();: PrimerIn 40% of the 162 countries evaluated, >25% of women who consumed any alcohol during pregnancy drank at 'bing...

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“…The IEC was compared with two other peptides that were shown neuroprotective. [22,23] The results show the probability of crossing the blood-brain barrier and entering the nerve center.…”

Section: Iec Binds Stably To the α-Synaptic Proteinsmentioning

confidence: 99%

Microalgae Octapeptide IIAVEAGC Alleviates Oxidative Stress and Neurotoxicity in 6‐OHDA‐Induced SH‐SY5Y Cells by Regulating the Nrf2/HO‐1and Jak2/Stat3 Pathways

Liu,

Lin,

Zheng

et al. 2024

Chemistry & Biodiversity

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Neurodegenerative diseases are characterized by the progressive loss of selectively vulnerable populations of neurons, and many factors are involved in its causes. Neurotoxicity and oxidative stress, are the main related factors. The octapeptide Ile‐Ile‐Ala‐Val‐Glu‐Ala‐Gly‐Cys (IEC) was identified from the microalgae Isochrysis zhanjiangensis and exhibited potential anti‐oxidative stress activity. In this study, the stability of α‐synaptic protein binding to IEC was modeled using molecular dynamics, and the results indicated binding stabilization within 60 ns. Oxidative stress in neurons is the major cause of α‐synaptic protein congestion. Therefore, we next evaluated the protective effects of IEC against oxidative stress and neurotoxicity in 6‐ohdainduced Parkinson’s disease (PD) model SH‐SY5Y cells in vitro. In oxidative stress, IEC appeared to increase the expression of the antioxidant enzymes HO‐1 and GPX through the antioxidant pathway of Nrf2, and molecular docking of IEC with Nrf2 and GPX could generate hydrogen bonds. Regarding apoptosis, IEC protected cells by increasing the Bcl‐2/Bax ratio, inhibiting the caspase cascade, acting on p53, and modulating the Jak2/Stat3 pathway. The results indicated that IEC exerted neuroprotective effects through the inhibition of α‐synaptic protein aggregation and antioxidant activity. Therefore, microalgal peptides have promising applications in the pre‐vention and treatment of neurodegenerative diseases.

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Neuroprotective Peptide NAPVSIPQ Antagonizes Ethanol Inhibition of L1 Adhesion by Promoting the Dissociation of L1 and Ankyrin-G

Cited by 9 publications

References 58 publications

Neuroprotective effect of miR-204-5p downregulation against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation

Neuroprotective effect of miR-204-5p downregulation against isoflurane-induced learning and memory impairment via targeting EphB2 and inhibiting neuroinflammation

Fetal alcohol spectrum disorders

Microalgae Octapeptide IIAVEAGC Alleviates Oxidative Stress and Neurotoxicity in 6‐OHDA‐Induced SH‐SY5Y Cells by Regulating the Nrf2/HO‐1and Jak2/Stat3 Pathways

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