scholarly journals Estradiol replacement evokes a wide range of transcriptional changes in the frontal cerebral cortex of middle-aged, ovariectomized rats

2011 ◽  
Vol 5 ◽  
Author(s):  
Liposits Z.
Keyword(s):  
Cerebral Cortex ◽  
Ovariectomized Rats ◽  
Middle Aged ◽  
Wide Range ◽  
Transcriptional Changes ◽  
Frontal Cerebral Cortex

scholarly journals Estradiol Replacement Alters Expression of Genes Related to Neurotransmission and Immune Surveillance in the Frontal Cortex of Middle-Aged, Ovariectomized Rats

Endocrinology ◽  
2010 ◽  
Vol 151 (8) ◽  
pp. 3847-3862 ◽  
Author(s):  
Miklós Sárvári ◽  
Imre Kalló ◽  
Erik Hrabovszky ◽  
Norbert Solymosi ◽  
Kinga Tóth ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Frontal Cortex ◽  
Expression Profiling ◽  
Hormone Replacement ◽  
Immune Surveillance ◽  
Ovariectomized Rats ◽  
Middle Aged ◽  
Wide Range ◽  
Frontal Cerebral Cortex ◽  
Genomic Effects

Estradiol (E2) modulates a wide range of functions of the frontal cerebral cortex. From the onset of menopause, declining levels of E2 can cause cognitive disturbances and changes in behavior that can be counterbalanced by hormone replacement. To study the effect of E2 replacement on the cortical transcriptome in a rodent model with low serum E2 level, we treated middle-aged, ovariectomized rats with E2 or vehicle using osmotic minipumps for 4 wk. Six animals for each group were selected, and samples of their frontal cortex were subjected to expression profiling using oligonucleotide microarrays. The explored E2-regulated genes were related to neurotransmission (Adora2a, Cartpt, Drd1a, Drd2, Gjb2, Nts, and Tac1), immunity (C3, C4b, Cd74, Fcgr2b, Mpeg1, and RT1-Aw2), signal transduction (Igf2, Igfbp2, Igfbp6, Rgs9, and Sncg), transport (Abca1, Hba-a2, Slc13a3, and Slc22a8), extracellular matrix (Col1a2, Col3a1, Fmod, and Lum), and transcription (Irf7 and Nupr1). Seventy-four percent of the transcriptional changes identified by microarray were confirmed by quantitative real-time PCR. The genes identified by expression profiling indicated that chronic E2 replacement significantly altered the transcriptome of the frontal cortex. The genomic effects of E2 influenced dopaminergic and peptidergic neurotransmission, immune surveillance, adenosine and insulin-like growth factor signaling and transport processes, among other functions. Identification of these novel E2-regulated mechanisms highlights the wide range of genomic responses of the aging female frontal cerebral cortex subjected to hormone replacement. Some of the genomic effects identified in this study may underlie the beneficial effects of E2 on cognition, behavior, and neuroprotection.

scholarly journals Role of CxxC-finger protein 1 in establishing mouse oocyte epigenetic landscapes

2021 ◽  
Author(s):  
Qian-Qian Sha ◽  
Ye-Zhang Zhu ◽  
Yunlong Xiang ◽  
Jia-Li Yu ◽  
Xiao-Ying Fan ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Histone H3 ◽  
Finger Protein ◽  
Maternal Genome ◽  
Wide Range ◽  
Transcriptional Changes ◽  
Nuclear Events ◽  
Genomic Regions ◽  
Cxxc Finger Protein 1

Abstract During oogenesis, oocytes gain competence and subsequently undergo meiotic maturation and prepare for embryonic development; trimethylated histone H3 on lysine-4 (H3K4me3) mediates a wide range of nuclear events during these processes. Oocyte-specific knockout of CxxC-finger protein 1 (CXXC1, also known as CFP1) impairs H3K4me3 accumulation and causes changes in chromatin configurations. This study investigated the changes in genomic H3K4me3 landscapes in oocytes with Cxxc1 knockout and the effects on other epigenetic factors such as the DNA methylation, H3K27me3, H2AK119ub1 and H3K36me3. H3K4me3 is overall decreased after knocking out Cxxc1, including both the promoter region and the gene body. CXXC1 and MLL2, which is another histone H3 methyltransferase, have nonoverlapping roles in mediating H3K4 trimethylation during oogenesis. Cxxc1 deletion caused a decrease in DNA methylation levels and affected H3K27me3 and H2AK119ub1 distributions, particularly at regions with high DNA methylation levels. The changes in epigenetic networks implicated by Cxxc1 deletion were correlated with the transcriptional changes in genes in the corresponding genomic regions. This study elucidates the epigenetic changes underlying the phenotypes and molecular defects in oocytes with deleted Cxxc1 and highlights the role of CXXC1 in orchestrating multiple factors that are involved in establishing the appropriate epigenetic states of maternal genome.

scholarly journals Effect of Handling on ATP Utilization of Cerebral Na,K-ATPase in rats with Trimethyltin-Induced Neurodegeneration.

2021 ◽  
Author(s):  
Barbora Kalocayova ◽  
Denisa Snurikova ◽  
Jana Vlkovicova ◽  
Veronika Navarova Stara ◽  
Dominika Michalikova ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Kinetic Properties ◽  
Potassium Ions ◽  
Catalytic Subunits ◽  
Key Enzyme ◽  
Male Wistar Rats ◽  
Frontal Cerebral Cortex ◽  
Α3 Subunit ◽  
The Brain ◽  
Sodium And Potassium

Abstract Previously it was shown that for reduction of anxiety and stress of experimental animals, preventive handling seems to be one of the most effective methods. The present study was oriented on Na,K-ATPase, a key enzyme for maintaining proper concentrations of intracellular sodium and potassium ions. Malfunction of this enzyme has an essential role in the development of neurodegenerative diseases. It is known that this enzyme requires approximately 50% of the energy available to the brain. Therefore in the present study utilization of the energy source ATP by Na,K-ATPase in the frontal cerebral cortex, using the method of enzyme kinetics was investigated. As a model of neurodegeneration treatment with Trimethyltin (TMT) was applied. Daily handling (10 min/day) of healthy rats and rats suffering neurodegeneration induced by administration of TMT in a dose of (7.5 mg/kg), at postnatal days 60-102 altered the expression of catalytic subunits of Na,K-ATPase as well as kinetic properties of this enzyme in frontal cerebral cortex of adult male Wistar rats. Everyday handling of rats, beside the previously published beneficial effect on spatial memory was accompanied by improwed maintenance of sodium homeeostasis in frontal cortex of brains. The key system responsible for this proces, the Na,K-ATPase was able to utilize better the energy substrate ATP. In rats with TMT-induced neurodegeneration handling promoted the expresion of α2 isoform of the enzyme which is typical for glial cells. In healthy rats the handling was followed by increased expression α3 subunit which is typical for neurons.

scholarly journals Frontal cerebral cortex blood flow, oxygen delivery and oxygenation during normoxic and hypoxic exercise in athletes

2011 ◽  
Vol 589 (16) ◽  
pp. 4027-4039 ◽  
Author(s):  
Ioannis Vogiatzis ◽  
Zafeiris Louvaris ◽  
Helmut Habazettl ◽  
Dimitris Athanasopoulos ◽  
Vasilis Andrianopoulos ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Oxygen Delivery ◽  
Frontal Cerebral Cortex ◽  
Hypoxic Exercise

Amyloidosis causes downregulation of SorLA, SorCS1 and SorCS3 expression in mice

2019 ◽  
Vol 400 (9) ◽  
pp. 1181-1189 ◽  
Author(s):  
Guido Hermey ◽  
Sabine A. Hoffmeister-Ullerich ◽  
Barbara Merz ◽  
Dagmar Groß ◽  
Dietmar Kuhl ◽  
...  
Keyword(s):  
Cerebral Cortex ◽  
Disease Progression ◽  
Amyloid Plaque ◽  
Plaque Formation ◽  
Amyloid Peptide ◽  
Subcellular Targeting ◽  
Altered Expression ◽  
Frontal Cerebral Cortex ◽  
Β Amyloid Peptide ◽  
A Minor

Abstract Accumulation of β-amyloid peptide (Aβ) is regarded as a primary cause of Alzheimer’s disease (AD). Aβ is derived by sequential cleavage of the amyloid precursor protein (APP). Alterations in the subcellular targeting of APP are thought to affect the degree of Aβ production. Sorting receptors, such as SorLA, convey subcellular targeting of APP. Dysfunction of SorLA, and likely of the related receptors SorCS1 and SorCS3, cause AD. Nevertheless, disease progression could also provoke altered expression of the receptors. Here, we assessed if Aβ plaque formation promotes altered expression of SorLA, SorCS1 and SorCS3. We analyzed transcript levels during aging and after amyloidosis in brain areas characterized by early amyloid plaque formation in an AD mouse model (APPPS1) and wild types. We observed stable expression levels during aging (1–12 months). After plaque formation, SorCS1 and SorLA expression were markedly reduced in the frontal cerebral cortex and to a minor extent in the hippocampus, whereas SorCS3 expression was solely reduced in the frontal cerebral cortex. Our results indicate that disease progression, associated with Aβ accumulation, can negatively regulate expression of the receptors.

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