Decreased expression of thyroid receptor-associated protein 220 in temporal lobe tissue of patients with refractory epilepsy

Wang, Xuefeng; Xi, Zhiqin; Gong, Yun; Liu, Fengying; Sun, Jijun; Wu, Yuan; Luan, Guoming; Wang, Yuping; Li, Yunlin; Zhang, Jianguo; Li, Hongwei

doi:10.1016/j.bbrc.2006.08.010

Cited by 16 publications

(11 citation statements)

References 31 publications

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“…Unfortunately, most patients who provided brain specimens were unwilling to provide the samples [ 63 ]. The observed reduction in the number of neurons after epilepsy is consistent with previous studies [ 65 , 66 , 67 ]. Therefore, a deficiency in fractalkine signaling is associated with many types of seizures [ 50 ].…”

Section: Cx3cl1/cxcr1 Signaling In Epilepsysupporting

confidence: 93%

The Impact of the CX3CL1/CX3CR1 Axis in Neurological Disorders

Pawelec

Ziemka‐Nałęcz

Sypecka

et al. 2020

Cells

135

116

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Fractalkine (FKN, CX3CL1) is a transmembrane chemokine expressed by neurons in the central nervous system (CNS). CX3CL1 signals through its unique receptor, CX3CR1, that is expressed in microglia. Within the CNS, fractalkine acts as a regulator of microglia activation in response to brain injury or inflammation. During the last decade, there has been a growing interest in the roles that the CX3CL1/CX3CR1 signaling pathway plays in the neuropathology of a diverse array of brain disorders. However, the reported results have proven controversial, indicating that a disruption of the CX3CL1 axis induces a disease-specific microglial response that may have either beneficial or detrimental effects. Therefore, it has become clear that the understanding of neuron-to-glia signals mediated by CX3CL1/CX3CR1 at different stages of diseases could provide new insight into potential therapeutic targets. Hence, the aim of this review is to provide a summary of the literature on the emerging role of CX3CL1 in animal models of some brain disorders.

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Section: Cx3cl1/cxcr1 Signaling In Epilepsysupporting

confidence: 93%

The Impact of the CX3CL1/CX3CR1 Axis in Neurological Disorders

Pawelec

Ziemka‐Nałęcz

Sypecka

et al. 2020

Cells

135

116

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“…Recent studies have shown that structurally normal brain tissue obtained from traumatic brain injury can be used as controls. 33,34 Secondly, μ-calpain’s involvement in the pathological process leading to causative or consequential epileptic seizures remains unclear. Based on the potential effects of μ-calpain on neuronal apoptosis, we hypothesize that its upregulation may play an important pathogenic role in the progression of IE.…”

Section: Discussionmentioning

confidence: 99%

Overexpression of μ-calpain in the anterior temporal neocortex of patients with intractable epilepsy correlates with clinicopathological characteristics

zhang

Hao

et al. 2011

Seizure

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Purpose This study aims to investigate μ-calpain expression profiles in the anterior temporal neocortex in patients with intractable epilepsy, and to determine whether its pattern of expression is related to pathological changes seen in these patients. Methods The study subjects consisted of 30 patients with intractable epilepsy and a control group of 10 patients with brain trauma who underwent resection of the anterior temporal lobe. μ-Calpain expression in surgically resected anterior temporal cortices of patients with intractable epilepsy were analyzed using the RT-PCR, Western blot, immnohistochemistry and immunofluorescence staining. GFAP expression was detected by immunohistochemical staining. The related pro-inflammatory cytokines were quantified by elisa. Clinicopathological characteristics were evaluated by HE staining. Results Analysis by Western blot and RT-PCR revealed that inactive μ-calpain expression and the calpain-cleaved spectrin fragment in surgically resected anterior temporal cortices of patients with intractable epilepsy were significantly increased compared to the tissues from corresponding regions of the control group. Immunohistological staining demonstrated that μ-calpain was overexpressed in the cell cytoplasm of neurons and glial cells in patients with intractable epilepsy and GFAP was overexpressed in the cell cytoplasm of glial cells in patients with intractable epilepsy. The level of pro-inflammatory cytokines, such as IL-1β, IL-6 and TGF-β1 were significantly increased in patients with intractable epilepsy. HE staining indicated μ-calpain overexpression is an independent prognostic factor for pathological changes such as neuronal loss, neuronal degeneration, gliosis and astrocytosis. Conclusion These data suggest that overexpression of μ-calpain is relationship with intractable epilepsy as well as the clinicopathological characteristics in these patients.

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“…The results showed that expression of TRAP220 mRNA in the temporal cortex was significantly reduced in epileptic patients both in mRNA and protein levels. This decrease might affect the pathophysiology of epilepsy and may be related to subsequent brain damage after frequent seizures [119,120].…”

Section: Page 16 Of 27mentioning

confidence: 99%

Thyroid hormones: Possible roles in epilepsy pathology

Tamijani

Karimi

Amini

et al. 2015

Seizure

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Thyroid hormones (THs) L-thyroxine and L-triiodothyronine, primarily known as metabolism regulators, are tyrosine-derived hormones produced by the thyroid gland. They play an essential role in normal central nervous system development and physiological function. By binding to nuclear receptors and modulating gene expression, THs influence neuronal migration, differentiation, myelination, synaptogenesis and neurogenesis in developing and adult brains. Any uncorrected THs supply deficiency in early life may result in irreversible neurological and motor deficits. The development and function of GABAergic neurons as well as glutamatergic transmission are also affected by THs. Though the underlying molecular mechanisms still remain unknown, the effects of THs on inhibitory and excitatory neurons may affect brain seizure activity. The enduring predisposition of the brain to generate epileptic seizures leads to a complex chronic brain disorder known as epilepsy. Pathologically, epilepsy may be accompanied by mitochondrial dysfunction, oxidative stress and eventually dysregulation of excitatory glutamatergic and inhibitory GABAergic neurotransmission. Based on the latest evidence on the association between THs and epilepsy, we hypothesize that THs abnormalities may contribute to the pathogenesis of epilepsy. We also review gender differences and the presumed underlying mechanisms through which TH abnormalities may affect epilepsy here.

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Decreased expression of thyroid receptor-associated protein 220 in temporal lobe tissue of patients with refractory epilepsy

Cited by 16 publications

References 31 publications

The Impact of the CX3CL1/CX3CR1 Axis in Neurological Disorders

The Impact of the CX3CL1/CX3CR1 Axis in Neurological Disorders

Overexpression of μ-calpain in the anterior temporal neocortex of patients with intractable epilepsy correlates with clinicopathological characteristics

Thyroid hormones: Possible roles in epilepsy pathology

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