Insulin induces neurite outgrowth via SIRT1 in SH-SY5Y cells

Liu, Y.; Yao, Zhigang; Zhang, L.; Zhu, Hua; Deng, Wei; Qin, Chuan

doi:10.1016/j.neuroscience.2013.01.034

Cited by 14 publications

(9 citation statements)

References 50 publications

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“…Cytoplasmic SIRT1 enhanced nerve growth factor-induced neuritogenesis in PC12 cells (Sugino et al, 2010 ). Insulin-induced neurite outgrowth of SH-SY5Y cells is dependent on SIRT1 (Liu et al, 2013b ). Primary neurons from transgenic mice overexpressing SIRT1 have enhanced neurite outgrowth and survival apparently via negative regulation of mammalian/mechanistic target of rapamyscin (mTOR) signaling (Guo et al, 2011 ).…”

Section: Sirt1 In Cns Neurons—role In Neurogenesis Neurite Growth Nementioning

confidence: 99%

SIRT1 in the brain—connections with aging-associated disorders and lifespan

Wijaya

Tang

2015

Front. Cell. Neurosci.

156

106

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The silent mating type information regulation 2 proteins (sirtuins) 1 of class III histone deacetylases (HDACs) have been associated with health span and longevity. SIRT1, the best studied member of the mammalian sirtuins, has a myriad of roles in multiple tissues and organs. However, a significant part of SIRT1’s role that impinges on aging and lifespan may lie in its activities in the central nervous system (CNS) neurons. Systemically, SIRT1 influences energy metabolism and circadian rhythm through its activity in the hypothalamic nuclei. From a cell biological perspective, SIRT1 is a crucial component of multiple interconnected regulatory networks that modulate dendritic and axonal growth, as well as survival against stress. This neuronal cell autonomous activity of SIRT1 is also important for neuronal plasticity, cognitive functions, as well as protection against aging-associated neuronal degeneration and cognitive decline. We discuss recent findings that have shed light on the various activities of SIRT1 in the brain, which collectively impinge on aging-associated disorders and lifespan.

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Section: Sirt1 In Cns Neurons—role In Neurogenesis Neurite Growth Nementioning

confidence: 99%

SIRT1 in the brain—connections with aging-associated disorders and lifespan

Wijaya

Tang

2015

Front. Cell. Neurosci.

156

106

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“…Insulin and its receptor have been implicated in neurite outgrowth and axon guidance, through activation of the PI3K/AKT pathway, as demonstrated in Drosophila (Song et al, 2003; Gu et al, 2014), murine (Grote et al, 2011) and human neuronal cells (Liu et al, 2013; Roloff et al, 2015). IRS p53 seems to play an essential role in dendritic arborization.…”

Section: Central Actions Of Insulinmentioning

confidence: 99%

Insulin and Autophagy in Neurodegeneration

et al. 2019

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Crosstalk in the pathophysiological processes underpinning metabolic diseases and neurodegenerative disorders have been the subject of extensive investigation, in which insulin signaling and autophagy impairment demonstrate to be a common factor in both conditions. Although it is still somewhat conflicting, pharmacological and genetic strategies that regulate these pathways may be a promising approach for aggregate protein clearancing and consequently the delaying of onset or progression of the disease. However, as the response due to this modulation seems to be time-dependent, finding the right regulation of autophagy may be a potential target for drug development for neurodegenerative diseases. In this way, this review focuses on the role of insulin signaling/resistance and autophagy in some neurodegenerative diseases, discussing pharmacological and non-pharmacological interventions in these diseases.

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“…SIRT1 shuttles between the cytoplasm and the nucleus [74], and could suppress neuronal death triggered by multiple stimuli via its deacetylation of TP53 [75,76,77] and the forkhead family of transcription factors [78,79,80]. Several reports have indicated that SIRT1 promotes neurite outgrowth in cultured neural cells [81,82,83], axonogenesis of primary neurons [84] and sensory axon regeneration of adult DRG neurons [85]. However, apart from the latter example, the first two mentioned study subjects were implicated in normal healthy morphological, developmental differentiation, rather than regeneration of damaged, degenerated, or cut axons after injury.…”

Section: Plausible Mechanistic Explanations For the Dichotomous Efmentioning

confidence: 99%

Why is NMNAT Protective against Neuronal Cell Death and Axon Degeneration, but Inhibitory of Axon Regeneration?

Tang

2019

Cells

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Nicotinamide mononucleotide adenylyltransferase (NMNAT), a key enzyme for NAD+ synthesis, is well known for its activity in neuronal survival and attenuation of Wallerian degeneration. Recent investigations in invertebrate models have, however, revealed that NMNAT activity negatively impacts upon axon regeneration. Overexpression of Nmnat in laser-severed Drosophila sensory neurons reduced axon regeneration, while axon regeneration was enhanced in injured mechanosensory axons in C. elegans nmat-2 null mutants. These diametrically opposite effects of NMNAT orthologues on neuroprotection and axon regeneration appear counterintuitive as there are many examples of neuroprotective factors that also promote neurite outgrowth, and enhanced neuronal survival would logically facilitate regeneration. We suggest here that while NMNAT activity and NAD+ production activate neuroprotective mechanisms such as SIRT1-mediated deacetylation, the same mechanisms may also activate a key axonal regeneration inhibitor, namely phosphatase and tensin homolog (PTEN). SIRT1 is known to deacetylate and activate PTEN which could, in turn, suppress PI3 kinase–mTORC1-mediated induction of localized axonal protein translation, an important process that determines successful regeneration. Strategic tuning of Nmnat activity and NAD+ production in axotomized neurons may thus be necessary to promote initial survival without inhibiting subsequent regeneration.

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Insulin induces neurite outgrowth via SIRT1 in SH-SY5Y cells

Cited by 14 publications

References 50 publications

SIRT1 in the brain—connections with aging-associated disorders and lifespan

SIRT1 in the brain—connections with aging-associated disorders and lifespan

Insulin and Autophagy in Neurodegeneration

Why is NMNAT Protective against Neuronal Cell Death and Axon Degeneration, but Inhibitory of Axon Regeneration?

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