Stem cell factor protects against neuronal apoptosis by activating AKT/ERK in diabetic mice

Li, J.-W.; Li, L.-L.; Chang, Ligong; Wang, Z.-Y.; Xu, Yitian

doi:10.1590/s0100-879x2009005000031

Cited by 19 publications

(9 citation statements)

References 27 publications

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“…For example, brain derived neurotrophic factor (BDNF) supports neuronal survival and plasticity [46] and is involved in learning and memory formation [47,48], while glial cell line-derived neurotrophic factor [49] [49] is neuroprotective [50,51], inhibits microglial activation [52] and promotes axonal regeneration [51,53]. TIMP-1, stem cell factor (SCF) and hepatocyte growth factor (HGF) also exhibit neuroprotective activities [54][55][56]. MMP-9 reduces the level of pathogenic Aβ oligomers in AD mice and restores synaptic and cognitive deficits in these mice [57], while transforming growth factor-β (TGF-β) modulates microglial activation [58].…”

Section: Discussionmentioning

confidence: 99%

Conditioned medium from the stem cells of human dental pulp improves cognitive function in a mouse model of Alzheimer’s disease

Mita

Furukawa‐Hibi

Takeuchi

et al. 2015

Behavioural Brain Research

136

118

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Section: Discussionmentioning

confidence: 99%

Conditioned medium from the stem cells of human dental pulp improves cognitive function in a mouse model of Alzheimer’s disease

Mita

Furukawa‐Hibi

Takeuchi

et al. 2015

Behavioural Brain Research

136

118

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“…We have found that in vitro IGF-I and SCF exert a cooperative neuroprotective effect against oxidative stress, suggesting that they may exert a similar beneficial role in vivo as after brain stroke both factors are upregulated in the lesioned area. Indeed, a cooperative neuroprotective effect of SCF with insulin has been reported 41 . The intracellular mechanisms mediating cooperation between these two factors involve Erk, a kinase activated by IGF-I.…”

Section: Discussionmentioning

confidence: 99%

Astrocytes require insulin-like growth factor I to protect neurons against oxidative injury

et al. 2014

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Oxidative stress is a proposed mechanism in brain aging, making the study of its regulatory processes an important aspect of current neurobiological research. In this regard, the role of the aging regulator insulin-like growth factor I (IGF-I) in brain responses to oxidative stress remains elusive as both beneficial and detrimental actions have been ascribed to this growth factor. Because astrocytes protect neurons against oxidative injury, we explored whether IGF-I participates in astrocyte neuroprotection and found that blockade of the IGF-I receptor in astrocytes abrogated their rescuing effect on neurons. The protection mediated by IGF-I against oxidative stress (H 2O 2) in astrocytes is probably needed for these cells to provide adequate neuroprotection. Indeed, in astrocytes but not in neurons, IGF-I helps decrease the pro-oxidant protein thioredoxin-interacting protein 1 and normalizes the levels of reactive oxygen species. Furthermore, IGF-I cooperates with trophic signals produced by astrocytes in response to H 2O 2 such as stem cell factor (SCF) to protect neurons against oxidative insult. After stroke, a condition associated with brain aging where oxidative injury affects peri-infarcted regions, a simultaneous increase in SCF and IGF-I expression was found in the cortex, suggesting that a similar cooperative response takes place in vivo. Cell-specific modulation by IGF-I of brain responses to oxidative stress may contribute in clarifying the role of IGF-I in brain aging.

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“…Baek et al have also reported that insulin withdrawal from HCN cells derived from adult rat brain induces autophagic cell death [274]. Elevation of cortical neuronal apoptosis in type 1 diabetic mice, reported by Li et al, is another evidence supporting the neuroprotective role of insulin [275]. On the other hand, hypothalamic neurosecretory cells are able to synthesize insulin, and it has been shown that, in older mice, the content of insulin in these cells is decreased.…”

Section: Protective Effects Against Apoptosismentioning

confidence: 93%

Insulin in the Brain: Sources, Localization and Functions

et al. 2012

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Historically, insulin is best known for its role in peripheral glucose homeostasis, and insulin signaling in the brain has received less attention. Insulin-independent brain glucose uptake has been the main reason for considering the brain as an insulin-insensitive organ. However, recent findings showing a high concentration of insulin in brain extracts, and expression of insulin receptors (IRs) in central nervous system tissues have gathered considerable attention over the sources, localization, and functions of insulin in the brain. This review summarizes the current status of knowledge of the peripheral and central sources of insulin in the brain, site-specific expression of IRs, and also neurophysiological functions of insulin including the regulation of food intake, weight control, reproduction, and cognition and memory formation. This review also considers the neuromodulatory and neurotrophic effects of insulin, resulting in proliferation, differentiation, and neurite outgrowth, introducing insulin as an attractive tool for neuroprotection against apoptosis, oxidative stress, beta amyloid toxicity, and brain ischemia.

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Stem cell factor protects against neuronal apoptosis by activating AKT/ERK in diabetic mice

Cited by 19 publications

References 27 publications

Conditioned medium from the stem cells of human dental pulp improves cognitive function in a mouse model of Alzheimer’s disease

Conditioned medium from the stem cells of human dental pulp improves cognitive function in a mouse model of Alzheimer’s disease

Astrocytes require insulin-like growth factor I to protect neurons against oxidative injury

Insulin in the Brain: Sources, Localization and Functions

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