Increased Expression of Rac1 in Epilepsy Patients and Animal Models

Li, Jie; Xing, Hongxia; Jiang, Guohui; Zhou, Shihao; Wu, Yuqing; Zhang, Yi; Guo, Shuangxi

doi:10.1007/s11064-015-1759-y

Cited by 10 publications

(6 citation statements)

References 38 publications

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“…Rho signaling is involved in several cerebral diseases, including intellectual disability (ID), epilepsy, drug addiction, HD, amyotrophic lateral sclerosis (ALS), and AD, and it acts by regulating axonogenesis, neuronal migration and synaptic plasticity (Table 3) (Mendoza-Naranjo et al, 2007; Locke et al, 2009; Zhang Y. et al, 2015; Li et al, 2016; Wang et al, 2017; Zimering, 2018; Costain et al, 2019). Rac1 and Rac3 are associated with intelligence by regulating key cellular functions in the central nervous system (Reijnders et al, 2017; Costain et al, 2019).…”

Section: The Rho Subfamily In Non-neoplastic Cerebral Diseasesmentioning

confidence: 99%

The Ras Superfamily of Small GTPases in Non-neoplastic Cerebral Diseases

Qu¹,

Pan²,

et al. 2019

Front. Mol. Neurosci.

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The small GTPases from the Ras superfamily play crucial roles in basic cellular processes during practically the entire process of neurodevelopment, including neurogenesis, differentiation, gene expression, membrane and protein traffic, vesicular trafficking, and synaptic plasticity. Small GTPases are key signal transducing enzymes that link extracellular cues to the neuronal responses required for the construction of neuronal networks, as well as for synaptic function and plasticity. Different subfamilies of small GTPases have been linked to a number of non-neoplastic cerebral diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), intellectual disability, epilepsy, drug addiction, Huntington's disease (HD), amyotrophic lateral sclerosis (ALS) and a large number of idiopathic cerebral diseases. Here, we attempted to make a clearer illustration of the relationship between Ras superfamily GTPases and non-neoplastic cerebral diseases, as well as their roles in the neural system. In future studies, potential treatments for non-neoplastic cerebral diseases which are based on small GTPase related signaling pathways should be explored further. In this paper, we review all the available literature in support of this possibility.

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Section: The Rho Subfamily In Non-neoplastic Cerebral Diseasesmentioning

confidence: 99%

The Ras Superfamily of Small GTPases in Non-neoplastic Cerebral Diseases

Qu¹,

Pan²,

et al. 2019

Front. Mol. Neurosci.

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“…Changes in the levels and activity of enzymes regulating the cytoskeleton such as Akt kinase, C-Abl kinase, and Rac1 small GTPase have also been reported in TLE patients but no evidence of pathogenicity has been forthcoming ( Chen et al. 2014 ; Li et al. 2016 ; Valmiki et al.…”

Section: Emerging Role Of the Cytoskeleton In Seizure Activity In Thementioning

confidence: 99%

Postnatal Role of the Cytoskeleton in Adult Epileptogenesis

Gavrilovici

Jiang

Kiroski

et al. 2020

Cerebral Cortex Communications

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Mutations in cytoskeletal proteins can cause early infantile and childhood epilepsies by misplacing newly born neurons and altering neuronal connectivity. In the adult epileptic brain, cytoskeletal disruption is often viewed as being secondary to aberrant neuronal activity and/or death, and hence simply representing an epiphenomenon. Here, we review the emerging evidence collected in animal models and human studies implicating the cytoskeleton as a potential causative factor in adult epileptogenesis. Based on the emerging evidence, we propose that cytoskeletal disruption may be an important pathogenic mechanism in the mature epileptic brain.

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“…A current study demonstrated that downregulated RAC1 decreased recurrent seizures in animal models of epilepsy, and found that RAC1-GTP was exclusively implicated in the mechanism of epilepsy (Li et al 2016). However, these authors did not further explore the upstream mechanism in reduced RAC1 activity in epilepsy and the downstream pathway of RAC1 in epilepsy also remains to be studied.…”

Section: The Challenge Of Microrna In Epilepsymentioning

confidence: 74%

The role of Rho/ROCK in epileptic seizure-related neuronal damage

2022

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Epilepsy is one of the most severe neurological disorders characterized by spontaneous recurrent seizures. Although more than two-thirds of patients can be cured with anti-epileptic drugs (AEDs), the rest one-third of epilepsy patients are resistant to AEDs. A series of studies have demonstrated Rho/Rho-associated kinase (ROCK) pathway might be involved in the pathogenesis of epilepsy in the recent twenty years. Several related pathway inhibitors of Rho/ROCK have been used in the treatment of epilepsy. We searched PubMed from Jan 1, 2000 to Dec 31, 2020, using the terms "epilepsy AND Rho AND ROCK" and "seizure AND Rho AND ROCK". We selected articles that characterized Rho/ROCK in animal models of epilepsy and patients. We then chose the most relevant research studies including in-vitro, in-vivo and clinical trials. The expression of Rho/ROCK could be a potential non-invasive biomarker to apply in treatment for patients with epilepsy. RhoA and ROCK show significant upregulation in the acute and chronic stage of epilepsy. ROCK inhibitors can reduce the epilepsy, epileptic seizure-related neuronal death and comorbidities. These findings demonstrate the novel development for diagnosis and treatment for patients with epilepsy. Rho/ROCK signaling pathway inhibitors may show more promising effects in epilepsy and related neurological diseases.

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Increased Expression of Rac1 in Epilepsy Patients and Animal Models

Cited by 10 publications

References 38 publications

The Ras Superfamily of Small GTPases in Non-neoplastic Cerebral Diseases

The Ras Superfamily of Small GTPases in Non-neoplastic Cerebral Diseases

Postnatal Role of the Cytoskeleton in Adult Epileptogenesis

The role of Rho/ROCK in epileptic seizure-related neuronal damage

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