Lead decreases cell survival, proliferation, and neuronal differentiation of primary cultured adult neural precursor cells through activation of the JNK and p38 MAP kinases

Engstrom, Anna K.; Wang, Hao; Xia, Zhengui

doi:10.1016/j.tiv.2015.05.001

Cited by 29 publications

(22 citation statements)

References 53 publications

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“…Moreover, the involvement of ERK in adult NSPC regulation was further confirmed by the observation that both differentiation and survival were inhibited after the deletion of the ERK5 kinase [132]. There is also evidence indicating that other members of the MAPK family such as c-Jun N-terminal kinase (JNK) and p38 take part in the proliferation, differentiation and survival of adult NSPCs [133], which, although not induced by addictive drugs, nonetheless suggests the existence of similar pathways in drug addiction.…”

Section: Common Mechanisms In Adult Nspc Regulationmentioning

confidence: 98%

Effects of addictive drugs on adult neural stem/progenitor cells

Loh

Law

2015

Cell. Mol. Life Sci.

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Neural stem/progenitor cells (NSPCs) undergo a series of developmental processes before giving rise to newborn neurons, astrocytes and oligodendrocytes in adult neurogenesis. During the past decade, the role of NSPCs has been highlighted by studies on adult neurogenesis modulated by addictive drugs. It has been proven that these drugs regulate the proliferation, differentiation and survival of adult NSPCs in different manners, which results in the varying consequences of adult neurogenesis. The effects of addictive drugs on NSPCs are exerted via a variety of different mechanisms and pathways, which interact with one another and contribute to the complexity of NSPC regulation. Here, we review the effects of different addictive drugs on NSPCs, and the related experimental methods and paradigms. We also discuss the current understanding of major signaling molecules, especially the putative common mechanisms, underlying such effects. Finally, we review the future directions of research in this area.

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Section: Common Mechanisms In Adult Nspc Regulationmentioning

confidence: 98%

Effects of addictive drugs on adult neural stem/progenitor cells

Loh

Law

2015

Cell. Mol. Life Sci.

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“…Once absorbed in the body lead, cadmium, and PCBs can influence brain functioning by affecting neural cells, inducing oxidative stress, and lowering dopamine concentrations [4–6]. Age-related decreases in cognitive functioning is typical as life progresses, mild cognitive impairment (MCI) is a greater than average age-related change in cognitive functioning [7].…”

Section: Introductionmentioning

confidence: 99%

A path analysis of multiple neurotoxic chemicals and cognitive functioning in older US adults (NHANES 1999–2002)

et al. 2017

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BackgroundPolychlorinated biphenyls (PCBs) and metals (lead and cadmium) are neurotoxic and affect neurobehavioral performance. Yet little is known about the association between exposure to multiple neurotoxic compounds and cognitive functioning in older adults.MethodsUsing data from two consecutive cycles of the National Health and Nutrition and Examination Survey (1999–2002), path analysis was used to simultaneously evaluate the association between whole blood concentrations of 14 neurotoxic compounds and cognitive functioning measured by the Digit Symbol Coding Test of the Weschler Adult Intelligence Scale, 3rd Edition in participants 60–84 years of age (N = 498). Effect modification was assessed for age (above/below the mean) and sex.ResultsThe final path model fit 5 compounds (i.e. PCB 74, PCB 118, PCB 146, PCB 153, and lead). After controlling for co-exposures and confounders, PCB 146 (β = −0.16, 95% CI: −0.29, −0.02, p = 0.02) and lead (β = −0.10, 95% CI: −0.20, −0.006, p = 0.04) were negatively associated with DSC scores in 60–84 year olds. Whereas, PCB 153 was positively associated with DSC scores (β =0.20, 95% CI: 0.05, 0.35; p = 0.01).ConclusionsThis cross-sectional analysis which controlled for collinear exposure to several neurotoxic compounds demonstrated an association between non-dioxin like polychlorinated biphenyl exposure, specifically PCB 146, and lower cognitive functioning, in older adults. Lead exposure was also weakly associated with lower cognitive functioning. Additional studies are needed to determine the causality of the observed associations.

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“…Wang et al 27) showed that exposure of the rat cortex to lead induced apoptosis through the MAPK signaling pathway by phosphorylation of ERK and JNK. In addition, Engstrom et al 28) reported that lead-induced neurotoxicity in neural precursor cells is mediated by the activation of JNK and p38 and inhibition of prosurvival Akt signaling. 28) In the present study, activation of ERK (Figs.…”

Section: +mentioning

confidence: 99%

“…In addition, Engstrom et al 28) reported that lead-induced neurotoxicity in neural precursor cells is mediated by the activation of JNK and p38 and inhibition of prosurvival Akt signaling. 28) In the present study, activation of ERK (Figs. 3A, 4) and p38 (Fig.…”

Section: +mentioning

confidence: 99%

Lead-Induced ERK Activation Is Mediated by GluR2 Non-containing AMPA Receptor in Cortical Neurons

Ishida

Kotake

Sanoh

et al. 2017

Biological & Pharmaceutical Bulletin

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Lead is a persistent environmental pollutant and exposure to high environmental levels causes various deleterious toxicities, especially to the central nervous system (CNS). The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor that is devoid of the glutamate receptor 2 (GluR2) subunit is Ca 2 -permeable, which increases the neuronal vulnerability to excitotoxicity. We have previously reported that long-term exposure of rat cortical neurons to lead acetate induces decrease of GluR2 expression. However, it is not clarified whether lead-induced GluR2 decrease is involved in neurotoxicity. Therefore, we investigated the contribution of GluR2 non-containing AMPA receptor to lead-induced neurotoxic events. Although the expression of four AMPA receptor subunits (GluR1, GluR2, GluR3, and GluR4) was decreased by lead exposure, the decrease in GluR2 expression was remarkable among four subunits. Lead-induced neuronal cell death was rescued by three glutamate receptor antagonists, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, a non-selective AMPA receptor blocker), MK-801 (N-methyl-D-aspartate (NMDA) receptor blocker), and 1-naphthyl acetyl spermine (NAS, a specific Ca 2 -permeable AMPA receptor blocker). Lead exposure activated extracellular signal-regulated protein kinase (ERK) 1/2, which was significantly ameliorated by CNQX. In addition, lead exposure activated p38 mitogen-activated protein kinase (MAPK p38), and protein kinase C (PKC), which was partially ameliorated by CNQX. Our findings indicate that Ca 2 -permeable AMPA receptors resulting from GluR2 decrease may be involved in lead-induced neurotoxicity.

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Lead decreases cell survival, proliferation, and neuronal differentiation of primary cultured adult neural precursor cells through activation of the JNK and p38 MAP kinases

Cited by 29 publications

References 53 publications

Effects of addictive drugs on adult neural stem/progenitor cells

Effects of addictive drugs on adult neural stem/progenitor cells

A path analysis of multiple neurotoxic chemicals and cognitive functioning in older US adults (NHANES 1999–2002)

Lead-Induced ERK Activation Is Mediated by GluR2 Non-containing AMPA Receptor in Cortical Neurons

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