Insulin attenuates arsenic-induced neurite outgrowth impairments by activating the PI3K/Akt/SIRT1 signaling pathway

Niyomchan, Apichaya; Watcharasit, Piyajit; Visitnonthachai, Daranee; Homkajorn, Benjaporn; Thiantanawat, Apinya; Satayavivad, Jutamaad

doi:10.1016/j.toxlet.2015.05.008

Cited by 17 publications

(12 citation statements)

References 32 publications

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“…Regarding Akt, two recent works highlighted its role in promoting neurite outgrowth [114,115]. The first demonstrated that Akt pathway activation by insulin is able to attenuate neurite outgrowth impairments induced by arsenic [114]; the second showed that Streptozotocin can be beneficial for neuronal cells inducing neurite outgrowth through activation of PI3K-Akt signaling pathway [115]. This is a N-nitrosourea natural compound discovered in a strain of Streptomyces achromogenes and originally identified as an antibiotic [116] On the other hand, it was found that the G3 domain of versican, one of the major extracellular matrix (ECM) proteins in the brain, stimulates ERK phosphorylation, enhancing neurite growth of hippocampal neurons [117].…”

Section: Role Of Egfr In Neurite Outgrowthmentioning

confidence: 99%

“…Akt and ERK are the main signaling pathways activated by EGFR and they are involved in neurite outgrowth ( Figure 6 D). Regarding Akt, two recent works highlighted its role in promoting neurite outgrowth [ 114 , 115 ]. The first demonstrated that Akt pathway activation by insulin is able to attenuate neurite outgrowth impairments induced by arsenic [ 114 ]; the second showed that Streptozotocin can be beneficial for neuronal cells inducing neurite outgrowth through activation of PI3K-Akt signaling pathway [ 115 ].…”

Section: Egfr Functions In the Cnsmentioning

confidence: 99%

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Role of EGFR in the Nervous System

Romanò

Bucci

2020

Cells

117

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Epidermal growth factor receptor (EGFR) is the first discovered member of the receptor tyrosine kinase superfamily and plays a fundamental role during embryogenesis and in adult tissues, being involved in growth, differentiation, maintenance and repair of various tissues and organs. The role of EGFR in the regulation of tissue development and homeostasis has been thoroughly investigated and it has also been demonstrated that EGFR is a driver of tumorigenesis. In the nervous system, other growth factors, and thus other receptors, are important for growth, differentiation and repair of the tissue, namely neurotrophins and neurotrophins receptors. For this reason, for a long time, the role of EGFR in the nervous system has been underestimated and poorly investigated. However, EGFR is expressed both in the central and peripheral nervous systems and it has been demonstrated to have specific important neurotrophic functions, in particular in the central nervous system. This review discusses the role of EGFR in regulating differentiation and functions of neurons and neuroglia. Furthermore, its involvement in regeneration after injury and in the onset of neurodegenerative diseases is examined.

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Section: Role Of Egfr In Neurite Outgrowthmentioning

confidence: 99%

Section: Egfr Functions In the Cnsmentioning

confidence: 99%

Role of EGFR in the Nervous System

Romanò

Bucci

2020

Cells

117

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“…Next, we examined EGFR-activated downstream signal transduction pathways involved in neurite outgrowth. Akt plays a role in promoting neurite outgrowth (Niyomchan et al, 2015; Nishimoto et al, 2016), which makes it a potential candidate. Immunoblotting result showed that in scrambled control, EGF treatment increased the phosphorylation level of Akt, which could be blocked by BIBX (Figures 6A,E–G).…”

Section: Resultsmentioning

confidence: 99%

Endocytic Adaptor Protein HIP1R Controls Intracellular Trafficking of Epidermal Growth Factor Receptor in Neuronal Dendritic Development

Yang

Peng

et al. 2018

Front. Mol. Neurosci.

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Huntington-interacting protein 1-related protein (HIP1R) was identified on the basis of its structural homology with HIP1. Based on its domain structure, HIP1R is a putative endocytosis-related protein. Our previous study had shown that knockdown of HIP1R induces a dramatic decrease of dendritic growth and branching in cultured rat hippocampal neurons. However, the underlying mechanism remains elucidative. In this study, we found that knockdown of HIP1R impaired the endocytosis of activated epidermal growth factor receptor (EGFR) and the consequent activation of the downstream ERK and Akt proteins. Meanwhile, it blocked the EGF-induced dendritic outgrowth. We also showed that the HIP1R fragment, amino acids 633–822 (HIP1R633–822), interacted with EGFR and revealed a dominant negative effect in disrupting the HIP1R-EGFR interaction-mediated neuronal development. Collectively, these results reveal a novel mechanism that HIP1R plays a critical role in neurite initiation and dendritic branching in cultured hippocampal neurons via mediating the endocytosis of EGFR and downstream signaling.

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“…10 Several studies reported that arsenic treatment shortened neurites. [11][12][13][14][15] Regarding the mechanisms involved in the inhibition of neurite extension, arsenic has been shown to decrease glutamate receptor subunit 1/2 levels, 12 suppress the LKB1/AMPK pathway, 15 and impair PI3K/Akt/SIRT1 signaling. 13 Recently, we demonstrated that prolonged arsenite treatment disrupted the neuronal insulin response.…”

mentioning

confidence: 99%

“…[11][12][13][14][15] Regarding the mechanisms involved in the inhibition of neurite extension, arsenic has been shown to decrease glutamate receptor subunit 1/2 levels, 12 suppress the LKB1/AMPK pathway, 15 and impair PI3K/Akt/SIRT1 signaling. 13 Recently, we demonstrated that prolonged arsenite treatment disrupted the neuronal insulin response. 16,17 Because IGF-1R and insulin receptor (IR) share common downstream signaling 18 and sodium arsenite-induced neurite shortening was attenuated by insulin, 13 this raised the question of whether sodium arseniteimpaired IGF-1 signaling consequently led to neurite retraction.…”

mentioning

confidence: 99%

Arsenic‐induced IGF‐1 signaling impairment and neurite shortening: The protective roles of IGF‐1 through the PI3K/Akt axis

Wisessaowapak,

Niyomchan,

Visitnonthachai

et al. 2023

Environmental Toxicology

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We recently reported that arsenic caused insulin resistance in differentiated human neuroblastoma SH‐SY5Y cells. Herein, we further investigated the effects of sodium arsenite on IGF‐1 signaling, which shares downstream signaling with insulin. A time‐course experiment revealed that sodium arsenite began to decrease IGF‐1‐stimulated Akt phosphorylation on Day 3 after treatment, indicating that prolonged sodium arsenite treatment disrupted the neuronal IGF‐1 response. Additionally, sodium arsenite decreased IGF‐1‐stimulated tyrosine phosphorylation of the IGF‐1 receptor β (IGF‐1Rβ) and its downstream target, insulin receptor substrate 1 (IRS1). These results suggested that sodium arsenite impaired the intrinsic tyrosine kinase activity of IGF‐1Rβ, ultimately resulting in a reduction in tyrosine‐phosphorylated IRS1. Sodium arsenite also reduced IGF‐1 stimulated tyrosine phosphorylation of insulin receptor β (IRβ), indicating the potential inhibition of IGF‐1R/IR crosstalk by sodium arsenite. Interestingly, sodium arsenite also induced neurite shortening at the same concentrations that caused IGF‐1 signaling impairment. A 24‐h IGF‐1 treatment partially rescued neurite shortening caused by sodium arsenite. Moreover, the reduction in Akt phosphorylation by sodium arsenite was attenuated by IGF‐1. Inhibition of PI3K/Akt by LY294002 diminished the protective effects of IGF‐1 against sodium arsenite‐induced neurite retraction. Together, our findings suggested that sodium arsenite‐impaired IGF‐1 signaling, leading to neurite shortening through IGF‐1/PI3K/Akt.

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Insulin attenuates arsenic-induced neurite outgrowth impairments by activating the PI3K/Akt/SIRT1 signaling pathway

Cited by 17 publications

References 32 publications

Role of EGFR in the Nervous System

Role of EGFR in the Nervous System

Endocytic Adaptor Protein HIP1R Controls Intracellular Trafficking of Epidermal Growth Factor Receptor in Neuronal Dendritic Development

Arsenic‐induced IGF‐1 signaling impairment and neurite shortening: The protective roles of IGF‐1 through the PI3K/Akt axis

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