Expression of FOXO transcription factors in the brain following traumatic brain injury

Li, Xilin; Gao, Chao-Chao; Qi, Min; Han, Yanling; Zhou, Meng-Liang; Zheng, Lan-rong

doi:10.1016/j.neulet.2021.135882

Cited by 12 publications

(14 citation statements)

References 25 publications

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“…FOXOs exert significant functions on the central nervous system and have an association with the maturation of neurons (Liu et al, 2021; Vezzali et al, 2016), among which changes in FOXO4 expression are involved in the onset and progression of EP seizures (Wang et al, 2017). In this study, we established the epilepsy animals (EPa) model to explore the impact of FOXO4 on hippocampal neuronal damage in EP mice.…”

Section: Discussionmentioning

confidence: 99%

FOXO4 alleviates hippocampal neuronal damage in epileptic mice via the miR‐138‐5p/ROCK2 axis

Jin

Liao

et al. 2022

American J of Med Genetics Pt B

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Epilepsy (EP) is one of the most universal neurological disorders. This study investigated the mechanism of forkhead box protein O4 (FOXO4) on hippocampal neuronal damage in EP mice. Initially, the EP mouse model and the in vitro HT-22 cell model were established. EP seizures and neuronal damage in mice were assessed. FOXO4, microRNA (miR)-138-5p, and rho-associated coiled-coil containing protein kinase 2 (ROCK2) levels in hippocampal tissues or HT-22 cells were examined. The cell viability and apoptosis of HT-22 cells were determined. The concentrations of oxidative stress markers and the levels of inflammatory cytokines in hippocampal tissues or HT-22 cells were detected. We found that FOXO4 was poorly expressed in EP. FOXO4 overexpression alleviated hippocampal neuronal damage in EP mice and improved HT-22 cell viability and inhibited apoptosis, and decreased oxidative stress and inflammation in hippocampal tissue and HT-22 cells. The bindings of miR-138-5p to FOXO4 and ROCK2 were analyzed, which showed that FOXO4 promoted miR-138-5p via binding to the miR-138-5p promoter region, and miR-138-5p inhibited ROCK2 expression. Joint experiments showed that miR-138-5p suppression or ROCK2 overexpression reversed the alleviation of FOXO4 overexpression on hippocampal neuronal damage. FOXO4 inhibited ROCK2 expression via promoting miR-138-5p expression, thus alleviating hippocampal neuronal damage in EP mice.

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Section: Discussionmentioning

confidence: 99%

FOXO4 alleviates hippocampal neuronal damage in epileptic mice via the miR‐138‐5p/ROCK2 axis

Jin

Liao

et al. 2022

American J of Med Genetics Pt B

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“…FoxOs are especially interesting since they can influence behavior and memory loss [18,203,309,316]. More than one hundred genes in the forkhead family and nine-teen human subgroups have been described.…”

Section: Mammalian Forkhead Transcription Factors and Multiple Sclerosismentioning

confidence: 99%

Cognitive Impairment in Multiple Sclerosis

Maiese

2023

Bioengineering

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Almost three million individuals suffer from multiple sclerosis (MS) throughout the world, a demyelinating disease in the nervous system with increased prevalence over the last five decades, and is now being recognized as one significant etiology of cognitive loss and dementia. Presently, disease modifying therapies can limit the rate of relapse and potentially reduce brain volume loss in patients with MS, but unfortunately cannot prevent disease progression or the onset of cognitive disability. Innovative strategies are therefore required to address areas of inflammation, immune cell activation, and cell survival that involve novel pathways of programmed cell death, mammalian forkhead transcription factors (FoxOs), the mechanistic target of rapamycin (mTOR), AMP activated protein kinase (AMPK), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), and associated pathways with the apolipoprotein E (APOE-ε4) gene and severe acute respiratory syndrome coronavirus (SARS-CoV-2). These pathways are intertwined at multiple levels and can involve metabolic oversight with cellular metabolism dependent upon nicotinamide adenine dinucleotide (NAD+). Insight into the mechanisms of these pathways can provide new avenues of discovery for the therapeutic treatment of dementia and loss in cognition that occurs during MS.

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“…FoxO activation during autophagy can be beneficial to cell survival, suggesting that a fine balance in FoxO activity may be required to promote cellular protection and survival. For example, FoxOs through the induction of autophagy can lead to the clearance of toxic intracellular accumulations and promote neuronal survival [203][204][205].…”

Section: Circadian Clock Genes and The Silent Mating Type Information Regulation 2 Homolog 1 (Saccharomyces Cerevisiae) (Sirt1)mentioning

confidence: 99%

Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways

Maiese

2021

Biomolecules

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Neurodegenerative disorders affect fifteen percent of the world’s population and pose a significant financial burden to all nations. Cognitive impairment is the seventh leading cause of death throughout the globe. Given the enormous challenges to treat cognitive disorders, such as Alzheimer’s disease, and the inability to markedly limit disease progression, circadian clock gene pathways offer an exciting strategy to address cognitive loss. Alterations in circadian clock genes can result in age-related motor deficits, affect treatment regimens with neurodegenerative disorders, and lead to the onset and progression of dementia. Interestingly, circadian pathways hold an intricate relationship with autophagy, the mechanistic target of rapamycin (mTOR), the silent mating type information regulation 2 homolog 1 (Saccharomyces cerevisiae) (SIRT1), mammalian forkhead transcription factors (FoxOs), and the trophic factor erythropoietin. Autophagy induction is necessary to maintain circadian rhythm homeostasis and limit cortical neurodegenerative disease, but requires a fine balance in biological activity to foster proper circadian clock gene regulation that is intimately dependent upon mTOR, SIRT1, FoxOs, and growth factor expression. Circadian rhythm mechanisms offer innovative prospects for the development of new avenues to comprehend the underlying mechanisms of cognitive loss and forge ahead with new therapeutics for dementia that can offer effective clinical treatments.

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Expression of FOXO transcription factors in the brain following traumatic brain injury

Cited by 12 publications

References 25 publications

FOXO4 alleviates hippocampal neuronal damage in epileptic mice via the miR‐138‐5p/ROCK2 axis

FOXO4 alleviates hippocampal neuronal damage in epileptic mice via the miR‐138‐5p/ROCK2 axis

Cognitive Impairment in Multiple Sclerosis

Cognitive Impairment and Dementia: Gaining Insight through Circadian Clock Gene Pathways

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