Identification of Gene Transcripts in Rat Frontal Cortex That Are Regulated by Repeated Electroconvulsive Seizure Treatment

Huang, Chih‐Ting; Chen, Chia‐Hsiang

doi:10.1159/000191123

Cited by 11 publications

(4 citation statements)

References 85 publications

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“…The following 12 hub genes were shared between the adipose tissue and the heart: ADRA1A (adrenoceptor alpha 1A), CCNF (cyclin F), CCR1 (C–C motif chemokine receptor 1), EGFR (epidermal growth factor receptor), MLYCD (malonyl-CoA decarboxylase), NRAS (NRAS proto-oncogene, GTPase), NSTR1 (neurotensin receptor 1), PRKCD , PTGFR (prostaglandin F receptor), SKP1 (S-phase kinase-associated protein 1), TTBK2 (tau tubulin kinase 2), and YKT6 ( Ykt6 v-Snare homolog). These hub genes can activate the calcium signaling pathway and promote the dysfunction of the heart and adipose tissue ( Huang and Chen, 2008 ; Li et al, 2008 ; Ye et al, 2014 ; Kao et al, 2015 ; Kuchay et al, 2017 ; Wang M. et al, 2018 ; Abe et al, 2020 ; da Silva Rosa et al, 2020 ; Esteves et al, 2020 ; Wu L. et al, 2020 ). CCR1 , which was downregulated in the adipose tissue but significantly upregulated in the heart, is directly associated with more than 10 other genes in the two tissues.…”

Section: Resultsmentioning

confidence: 99%

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

et al. 2021

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Heart failure with preserved ejection fraction (HFpEF) is a complex disease characterized by dysfunctions in the heart, adipose tissue, and cerebral arteries. The elucidation of the interactions between these three tissues in HFpEF will improve our understanding of the mechanism of HFpEF. In this study, we propose a multilevel comparative framework based on differentially expressed genes (DEGs) and differentially correlated gene pairs (DCGs) to investigate the shared and unique pathological features among the three tissues in HFpEF. At the network level, functional enrichment analysis revealed that the networks of the heart, adipose tissue, and cerebral arteries were enriched in the cell cycle and immune response. The networks of the heart and adipose tissues were enriched in hemostasis, G-protein coupled receptor (GPCR) ligand, and cancer-related pathway. The heart-specific networks were enriched in the inflammatory response and cardiac hypertrophy, while the adipose-tissue-specific networks were enriched in the response to peptides and regulation of cell adhesion. The cerebral-artery-specific networks were enriched in gene expression (transcription). At the module and gene levels, 5 housekeeping DEGs, 2 housekeeping DCGs, 6 modules of merged protein–protein interaction network, 5 tissue-specific hub genes, and 20 shared hub genes were identified through comparative analysis of tissue pairs. Furthermore, the therapeutic drugs for HFpEF-targeting these genes were examined using molecular docking. The combination of multitissue and multilevel comparative frameworks is a potential strategy for the discovery of effective therapy and personalized medicine for HFpEF.

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Section: Resultsmentioning

confidence: 99%

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

et al. 2021

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“…YKT6 codes for an evolutionary conserved SNARE essential for ER-Gogi transport, highly expressed in neurons and enriched in hippocampus [ 141 ]. YKT6 is co-upregulated with S100B (a VIP in L-CO network, module C) upon seizures [ 142 ]. SERPINB2 is one of the nine hippocampal core genes for synaptic activity-induced neuroprotection against seizure-induced brain-damage [ 143 ].…”

Section: Resultsmentioning

confidence: 99%

Community Structure Analysis of Transcriptional Networks Reveals Distinct Molecular Pathways for Early- and Late-Onset Temporal Lobe Epilepsy with Childhood Febrile Seizures

et al. 2015

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Age at epilepsy onset has a broad impact on brain plasticity and epilepsy pathomechanisms. Prolonged febrile seizures in early childhood (FS) constitute an initial precipitating insult (IPI) commonly associated with mesial temporal lobe epilepsy (MTLE). FS-MTLE patients may have early disease onset, i.e. just after the IPI, in early childhood, or late-onset, ranging from mid-adolescence to early adult life. The mechanisms governing early (E) or late (L) disease onset are largely unknown. In order to unveil the molecular pathways underlying E and L subtypes of FS-MTLE we investigated global gene expression in hippocampal CA3 explants of FS-MTLE patients submitted to hippocampectomy. Gene coexpression networks (GCNs) were obtained for the E and L patient groups. A network-based approach for GCN analysis was employed allowing: i) the visualization and analysis of differentially expressed (DE) and complete (CO) - all valid GO annotated transcripts - GCNs for the E and L groups; ii) the study of interactions between all the system’s constituents based on community detection and coarse-grained community structure methods. We found that the E-DE communities with strongest connection weights harbor highly connected genes mainly related to neural excitability and febrile seizures, whereas in L-DE communities these genes are not only involved in network excitability but also playing roles in other epilepsy-related processes. Inversely, in E-CO the strongly connected communities are related to compensatory pathways (seizure inhibition, neuronal survival and responses to stress conditions) while in L-CO these communities harbor several genes related to pro-epileptic effects, seizure-related mechanisms and vulnerability to epilepsy. These results fit the concept, based on fMRI and behavioral studies, that early onset epilepsies, although impacting more severely the hippocampus, are associated to compensatory mechanisms, while in late MTLE development the brain is less able to generate adaptive mechanisms, what has implications for epilepsy management and drug discovery.

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“…The presented recognition-behavioral stresscoping glycolipids would promote synaptic plasticity in the corresponding neuronal modules. In fact, both of the repeated electroconvulsive treatment for major depression patients and the lithium carbonate medication for mania patients increase the synaptic plasticity [22,23]. Now, the stresscoping glycolipids are produced via the gene expressions.…”

Section: Discussionmentioning

confidence: 99%

Recognition-behavioral stress-coping humoral glycolipids produced by medicated major psychoses patients

Masuda¹

2019

Preprint

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Background Mammalians have the recognition-behavioral stress-coping system regulated via the neuronal modules followed by some humoral glycolipids. A sulfated Galbeta1-4GlcNAc-lipid promotes the serotonergic module. GalNAcalpha1-3GalNAc-lipid promotes the adrenergic module. A Fucalpha1-2Glc-lipid protects the cholinergic module. Sialalpha2-3Gal-lipid promotes the dopaminergic module.Methods Major psychoses patients show the emotional and recognition-behavioral symptoms, and long-time medication does not completely delete the symptoms. I examined the recognitionbehavioral stress-coping humoral glycolipids produced by medicated major psychoses patients. ResultsThe major depression patients produced the sulfated Galbeta1-4GlcNAc-lipid and the sulfated Fucalpha1-2Glc-lipid, but deduced the GalNAcalpha1-3GalNAc-lipid. The mania patients produced the sulfated Galbeta1-4GlcNAc-lipid. The schizophrenia patients produced the sulfated Galbeta1-4GlcNAclipid, and remarkably produced the Sialalpha2-3Gal-lipid. Ruled out the medication-effects, the major depression patients decreased the serotonergic module function and the adrenergic module function, but increased the cholinergic module function. The mania patients increased the serotonergic module function and the adrenergic module function. The schizophrenia patients increased the serotonergic module function, and particularly increased the dopaminergic module function.Conclusion These suggest the stress-coping humoral glycolipids produced by the patients corresponded to the symptoms. Furthermore, I understood the humoral Sialalpha2-3Gal-lipid would be considered as another biomarker identifying schizophrenia.

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Identification of Gene Transcripts in Rat Frontal Cortex That Are Regulated by Repeated Electroconvulsive Seizure Treatment

Cited by 11 publications

References 85 publications

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

Multiple-Tissue and Multilevel Analysis on Differentially Expressed Genes and Differentially Correlated Gene Pairs for HFpEF

Community Structure Analysis of Transcriptional Networks Reveals Distinct Molecular Pathways for Early- and Late-Onset Temporal Lobe Epilepsy with Childhood Febrile Seizures

Recognition-behavioral stress-coping humoral glycolipids produced by medicated major psychoses patients

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