Proneurotrophins, Seizures, and Neuronal Apoptosis

Friedman, Wilma J.

doi:10.1177/1073858409349903

Cited by 66 publications

(53 citation statements)

References 70 publications

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“…Much research in recent years has indicated that the occurrence of epilepsy is closely related to the disruption of a variety of cerebral apoptosis genes (Friedman, 2010). Our experiments found the increased expression of apoptosis related factors, such as FASLG and FOS, indicating that the abnormal activation of mTOR-mediated apoptosis may be involved in the epileptogenic mechanisms of type II FCD-related epilepsy, which is consistent with the experimental results of Iyer et al (2014).…”

Section: Discussionsupporting

confidence: 91%

PI3K-AKT pathway polymerase chain reaction (PCR) array analysis of epilepsy induced by type II focal cortical dysplasia

Lin¹,

Lin²,

Liu³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The aims of this study were to observe the differential expression of PI3K-AKT pathway-related genes in seizure-inducing brain lesions in type II focal cortical dysplasia, and to explore the relationship between gene expression and histological changes in dysplastic foci and their epileptogenic mechanism. Typical lesions in brain tissue from three patients with epilepsy induced by type II focal cortical dysplasia were selected for analysis, along with normal brain tissue from two control group individuals. Following quantitative expression analysis using the RT2 Profiler TM PI3K-AKT PCR Array, differential expression of the pathway related genes was detected in the focal brain tissue lesions, and gene function queries were performed. Compared with the control group, thirteen related genes appeared to exhibit marked differences in expression in epileptic lesions from (2015) patients with type II focal cortical dysplasia; those genes were found to be involved in regulation of cell size, morphology, adhesion, migration, and apoptosis, and in immunity, inflammation, and many other domains. The differential expression of multiple genes in the PI3K-AKT signaling pathway in type II focal cortical dysplasia may be an important molecular mechanism underlying histological changes and recurrent seizures.

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Section: Discussionsupporting

confidence: 91%

PI3K-AKT pathway polymerase chain reaction (PCR) array analysis of epilepsy induced by type II focal cortical dysplasia

Lin¹,

Lin²,

Liu³

et al. 2015

Genet. Mol. Res.

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“…The Trk receptors are mostly responsible for the maturation of neurotrophins and promote survival and differentiation of neurons as well as the synaptic function. 50 It was reported recently that in the absence of its ligand, the TrkC receptor can induce apoptosis in various cell lines. 51 Furthermore, in contrast to mature neurotrophins, their predecessors can drive the apoptotic processes via the complex of p75NTR and sortilin.…”

Section: Discussionmentioning

confidence: 99%

Identification of functional networks associated with cell death in the retina of OXYS rats during the development of retinopathy

et al. 2015

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Age-related macular degeneration (AMD) is a major cause of blindness in developed countries, and the molecular pathogenesis of early events in AMD is poorly understood. Senescence-accelerated OXYS rats develop AMD-like retinopathy. The aim of this study was to explore the differences in retinal gene expression between OXYS and Wistar (control) rats at age 20 d and to identify the pathways of retinal cell death involved in the OXYS retinopathy initiation and progression. Retinal mRNA profiles of 20-day-old OXYS and Wistar rats were generated at the sequencing read depth 40 mln, in triplicate, using Illumina GAIIx. A terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling (TUNEL) assay was performed to measure the apoptosis level. GeneMANIA was used to construct interaction networks for differentially expressed (DE) apoptosis-related genes at ages 20 d and 3 and 18 months. Functional analysis was suggestive of a developmental process, signal transduction, and cell differentiation as the most enriched biological processes among 245 DE genes at age 20 d An increased level of apoptosis was observed in OXYS rats at age 20 d but not at advanced stages. We identified functional clusters in the constructed interaction networks and possible hub genes (Rasa1, cFLAR, Birc3, Cdk1, Hspa1b, Erbb3, and Ntf3). We also demonstrated the significance of the extrinsic apoptotic pathway at preclinical, early, and advanced stages of retinopathy development. Besides the cell death signaling pathways, immune system-related processes and lipid-metabolic processes showed overrepresentation in the clusters of all networks. These characteristics of the expression profile of the genes functionally associated with apoptosis may contribute to the pathogenesis of AMD-like retinopathy in senescence-accelerated OXYS rats.

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“…Hence, dosing of NTs could greatly effect nerve regeneration, in some cases and present a challenge for NT treatments after nerve injury. On the other hand, pro-neurotrophins have gained recognition for contributing to apoptosis (Freidman 2010). Pro-neurotrophins are uncleaved neurotrophin precursors which can be secreted by neurons and glia.…”

Section: Challenges For Nt Treaments After Injurymentioning

confidence: 99%

Neurotrophin treatment to promote regeneration after traumatic CNS injury

Kelamangalath

Smith

2013

Front. Biol.

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Neurotrophins are a family of growth factors that have been found to be central for the development and functional maintenance of the nervous system, participating in neurogenesis, neuronal survival, axonal growth, synaptogenesis and activity-dependent forms of synaptic plasticity. Trauma in the adult nervous system can disrupt the functional circuitry of neurons and result in severe functional deficits. The limitation of intrinsic growth capacity of adult nervous system and the presence of an inhospitable environment are the major hurdles for axonal regeneration of lesioned adult neurons. Neurotrophic factors have been shown to be excellent candidates in mediating neuronal repair and establishing functional circuitry via activating several growth signaling mechanisms including neuron-intrinsic regenerative programs. Here, we will review the effects of various neurotrophins in mediating recovery after injury to the adult spinal cord.

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Proneurotrophins, Seizures, and Neuronal Apoptosis

Cited by 66 publications

References 70 publications

PI3K-AKT pathway polymerase chain reaction (PCR) array analysis of epilepsy induced by type II focal cortical dysplasia

PI3K-AKT pathway polymerase chain reaction (PCR) array analysis of epilepsy induced by type II focal cortical dysplasia

Identification of functional networks associated with cell death in the retina of OXYS rats during the development of retinopathy

Neurotrophin treatment to promote regeneration after traumatic CNS injury

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