RETRACTED ARTICLE: Developmental changes in Notch1 and NLE1 expression in a genetic model of absence epilepsy

Karimzadeh, Fariba; Mousavi, Sayed Mostafa Modarres; Alipour, Fatemeh; Ravandi, Hassan Hosseini; Kovač, Stjepana; Gorji, Ali

doi:10.1007/s00429-017-1371-9

Cited by 16 publications

(13 citation statements)

References 44 publications

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“…Botch, NPG7, was identified in functional screen for neuroprotective proteins, and there are previous studies on the correlation between Botch and the Notch1 signaling pathway [ 6 , 22 ]. It is generally accepted that Notch1 plays a critical role in many fundamental processes and in a wide range of tissues, and it is not surprising that aberrant gain or loss of Notch1 signaling components has been directly linked to differentiation, proliferation, inflammation and apoptosis [ 13 , 18 – 21 , 27 ]. Yet, none of these studies have elucidated whether Botch could involve in the brain protection against ICH-induced SBI through its suppression effects of Notch1.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotection of Botch in experimental intracerebral hemorrhage in rats

Mei

Zhu

et al. 2017

Oncotarget

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Notch1 maturation participates in apoptosis and inflammation following intracerebral hemorrhage (ICH). It has been reported that Botch bound to and blocked Notch1 maturation. Here we estimated the role of Botch in ICH-induced secondary brain injury and underlying mechanisms. Experimental ICH model was induced by autologous arterial blood injection in Sprague-Dawley rats, and cultured primary rat cortical neurons were exposed to oxyhemoglobin to mimic ICH in vitro. Specific small interfering RNAs and expression plasmids encoding wild type Botch and Botch with Glu115Ala mutation were exploited. The protein levels of Botch and Notch1 transmembrane intracellular domain (Notch1-TMIC) were increased within brain tissue around hematoma. Botch overexpression led to an increase in unprocessed Notch1 full-length form accompanied by a significant decrease in Notch1-TMIC, while Botch knockdown resulted in an approximately 1.5-fold increase in Notch1-TMIC. There were increased cell apoptosis, necrosis and neurobehavioral deficits after ICH, which was inhibited by Botch overexpression and enhanced by Botch knockdown. Double immunofluorescence showed a colocalization of Botch and Notch1 in the trans-Golgi. Overexpression of wild type Botch, but not Botch E115A mutant, led to an increase in the interaction between Botch and Notch1, reduced the formation and the nuclear localization of Notch1 intracellular domain, and attenuated cell apoptosis and inflammation. In conclusion, Botch exerts neuroprotection against neuronal damage via antagonizing the maturation of Notch1 in Glu115-denpendent manner. However, neuroprotection mediated by endogenous Botch is not enough to reverse ICH-induced secondary brain injury.

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Section: Discussionmentioning

confidence: 99%

Neuroprotection of Botch in experimental intracerebral hemorrhage in rats

Mei

Zhu

et al. 2017

Oncotarget

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“…In addition, we had shown the lack of GFAP expression in the different cortical layers in the WAG/Rij rats (Karimzadeh et al, 2017).…”

Section: Cortical Expressionmentioning

confidence: 91%

Alteration in Neuregulin 1/ERbB4 in Absence Epilepsy: Regulatory Effect on TRPV1 Expression

Talebi¹,

Ghorbani²,

Alizadeh³

et al. 2022

BCN

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The footprint of Neuregulin 1 (NRG1) / ERbB4 in the pathophysiology of some neurological disorders and TRPV1 regulation has been indicated. The alterations of NRG1 and ErbB4 as well as TRPV1 signaling pathway was investigated during development of absence epilepsy in the genetic animal model of absence epilepsy. Male WAG/Rij and Wistar rats were divided into four experimental groups of 2 and 6 months of age. The protein level of NRG1, ERbB4 and TRPV1 were measured in the somatosensory cortex and hippocampus. The cortical protein level of NRG1 and ErbB4 in the 6-month-old WAG/Rij rats was lower than Wistar rats. Protein level of TRPV1 was lower in 2- and 6-month-old WAG/Rij rats compared to age-matched Wistar rats. Hippocampal protein level of NRG1 in 6-month-old WAG/Rij rats was lower than 2-month-old WAG/Rij rats. Low level of ErbB4 protein in 2-month-old and high level in 6-month-old WAG/Rij rats was shown compared to Wistar rats. Protein level of TRPV1 was lower in the 2-month-old and higher in 6-month- old WAG/Rij rats compared to age-matched Wistar rats. Furthermore, high correlation between NRG1/ERbB4 and TRPV1 expressions in the cortex and hippocampus was indicated. The expression of NRG1/ERbB4 and TRPV1 followed a similar pattern during life span of Wistar and WAG/Rij rats.Our findings indicated the potential role of NRG1/ErbB4 pathway as well as TRPV1 in the pathogenesis of absence epilepsy. The regulatory effect of ERbB4 receptor on the TRPV1 expression has been suggested following by the similarity pattern of expression.

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“…Six rats of each experimental group were deeply anaesthetized by chloralhydrate and perfused transcardially with 200 ml of saline followed by 600 ml of 4% paraformaldehyde (PFA) solution. The brains were extracted and kept in 4% PFA for at least 4 days at 4°C (Karimzadeh, Mousavi, Alipour, et al, 2017). The paraffin embedded series of 8-µm-thick coronal sections were cut every 100 µm from 1.8 to 4.3 mm posterior to the bregma (Paxinos & Watson, 2007).…”

Section: Immunofluorescent Analysismentioning

confidence: 99%

“…Recombinant protein of Jagged1 was dissolved 10 µg/1 µl PBS. DAPT was dissolved in DMSO and with concentration of 50 µM was administrated (Karimzadeh, Mousavi, Alipour, et al, 2017;Sha et al, 2014).…”

Section: Immunofluorescent Analysismentioning

confidence: 99%

Discrepancies of Notch 1 receptor during development of chronic seizures

Saffarzadeh

Mousavi

Lotfinia

et al. 2019

Journal Cellular Physiology

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The critical role of Notch signaling has been shown in the pathogenesis of some neurological disorders including schizophrenia, epilepsy and Alzheimer’s disease. This study was aimed to evaluate the role of Notch 1 receptor in epileptogenesis as well as seizure characteristics. The animals were divided into three groups of sham, early stage and end stage. In sham group: Normal saline was injected intraperitoneally (ip) in the same as protocol of pentylenetetrazol (PTZ) injection. PTZ was injected (ip) every 48 hr over a period of 1 week in the group of early stage and over a period of 4 weeks in the end stage. The gene expression as well as distribution of Notch 1 receptor was assessed in the parietal cortex and hippocampus. In addition, the effect of agonist or antagonist of Notch 1 receptor was assessed on the epileptic discharges induced by PTZ injection. The gene expression of Notch 1 decreased in the hippocampus significantly in the end‐stage group compared with sham, and early groups. Furthermore, distribution of Notch 1 receptor increased in the somatosensory cortex and decreased in the CA1 hippocampal area in the end‐stage group. Intraventricular microinjection of Notch 1 agonist significantly increased the amplitude as well as frequency of spikes and decreased the latency of first epileptic discharges. Our findings illustrate the critical role of Notch signalling as a potential pathway in the epileptogenesis during development of chronic seizures.

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RETRACTED ARTICLE: Developmental changes in Notch1 and NLE1 expression in a genetic model of absence epilepsy

Cited by 16 publications

References 44 publications

Neuroprotection of Botch in experimental intracerebral hemorrhage in rats

Neuroprotection of Botch in experimental intracerebral hemorrhage in rats

Alteration in Neuregulin 1/ERbB4 in Absence Epilepsy: Regulatory Effect on TRPV1 Expression

Discrepancies of Notch 1 receptor during development of chronic seizures

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