scholarly journals Changes in expression of GFAP, ApoE and APP mRNA and protein levels in the adult rat brain following cortical injury

2013 ◽  
Vol 65 (1) ◽  
pp. 255-264
Author(s):  
Natasa Loncarevic-Vasiljkovic ◽  
Vesna Pesic ◽  
N. Tanic ◽  
Desanka Milanovic ◽  
Aleksandra Mladenovic-Djordjevic ◽  
...  
Keyword(s):  
Brain Plasticity ◽  
Recovery Period ◽  
Potential Contribution ◽  
Cortical Injury ◽  
Adult Rat ◽  
Protein Levels ◽  
Adult Rat Brain ◽  
Apoe Protein ◽  
The Brain

The recovery period following cortical injury (CI) is characterized by a dynamic and highly complex interplay between beneficial and detrimental events. The aim of this study was to examine the expressions of Glial Fibrillary Acidic Protein (GFAP), Apolipoprotein E (ApoE) and Amyloid Precursor Protein (APP), all of which are involved in brain plasticity and neurodegeneration. Our results reveal that CI strongly influenced GFAP, ApoE and APP mRNA expression, as well as GFAP and ApoE protein expression. Considering the pivotal role of these proteins in the brain, the obtained results point to their potential contribution in neurodegeneration and consequent Alzheimer?s disease development.

scholarly journals The distribution of oxytocin and the oxytocin receptor in rat brain: relation to regions active in migraine

2020 ◽  
Vol 21 (1) ◽  
Author(s):  
Karin Warfvinge ◽  
Diana Krause ◽  
Lars Edvinsson
Keyword(s):  
Rat Brain ◽  
Nerve Fibers ◽  
Adult Rat ◽  
Paraventricular Nuclei ◽  
Hypothalamic Nuclei ◽  
Calcitonin Gene ◽  
Adult Rat Brain ◽  
Central Actions ◽  
The Brain

Abstract Background Recent work, both clinical and experimental, suggests that the hypothalamic hormone oxytocin (OT) and its receptor (OTR) may be involved in migraine pathophysiology. In order to better understand possible central actions of OT in migraine/headache pathogenesis, we mapped the distribution of OT and OTR in nerve cells and fibers in rat brain with a focus on areas related to migraine attacks and/or shown previously to contain calcitonin gene related peptide (CGRP), another neuropeptide involved in migraine. Methods Distribution of OT and OTR in the adult, rat brain was qualitatively examined with immunohistochemistry using a series of well characterized specific antibodies. Results As expected, OT was extensively localized in the cell somas of two hypothalamic nuclei, the supraoptic (SO or SON) and paraventricular nuclei (Pa or PVN). OT also was found in many other regions of the brain where it was localized mainly in nerve fibers. In contrast, OTR staining in the brain was mainly observed in cell somas with very little expression in fibers. The most distinct OTR expression was found in the hippocampus, the pons and the substantia nigra. In some regions of the brain (e.g. the amygdala and the hypothalamus), both OT and OTR were expressed (match). Mismatch between the peptide and its receptor was primarily observed in the cerebral and cerebellar cortex (OT expression) and hippocampus (OTR expression). Conclusions We compared OT/OTR distribution in the CNS with that of CGRP and identified regions related to migraine. In particular, regions suggested as “migraine generators”, showed correspondence among the three mappings. These findings suggest central OT pathways may contribute to the role of the hypothalamus in migraine attacks.

scholarly journals Особливості масометричних показників та морфологічних змін головного мозку статевозрілих щурів в умовах впливу на організм сульфатів міді, цинку та заліза

2015 ◽  
Author(s):  
А. М. Романюк ◽  
Г. Ю Будко
Keyword(s):  
Copper Sulfate ◽  
Morphological Changes ◽  
The Body ◽  
Male Rats ◽  
Relative Mass ◽  
Adult Rat ◽  
Applied Anatomy ◽  
Adult Rat Brain ◽  
Long Acting ◽  
The Brain

ОСОБЛИВОСТІ МАСОМЕТРИЧНИХ ПОКАЗНИКІВ ТА МОРФОЛОГІЧНИХ ЗМІН ГОЛОВНОГО МОЗКУ СТАТЕВОЗРІЛИХ ЩУРІВ В УМОВАХ ВПЛИВУ НА ОРГАНІЗМ СУЛЬФАТІВ МІДІ, ЦИНКУ ТА ЗАЛІЗА - З метою вивчення масометричних показників щурів та їх головного мозку за умов довготривалої дії (упродовж 90 діб) на організм сульфатів міді, цинку та заліза було проведено експеримент на 48 білих статевозрілих щурах-самцях масою 200-250 г віком 5-7 місяців. Застосовували анатомічні, статистичні та загальноприйняті методики мікроанатомічного методу дослідження. Встановлено, що комбінований вплив на організм сульфатів міді цинку та заліза чинить на головний мозок досить виражений токсичний ефект, що негативно позначається на масометричних показниках загальної маси щурів та маси головного мозку. Це свідчить про розвиток у головному мозку явищ гострого набряку з ознаками геморагічної інфільтрації. Ступінь вираження набряку зростає та досягає максимальних показників наприкінці експерименту.<br />ОСОБЕННОСТИ МАСОМЕТРИЧЕСКИХ ПОКАЗАТЕЛЕЙ И МОРФОЛОГИЧЕСКИХ ИЗМЕНЕНИЙ ГОЛОВНОГО МОЗГА ПОЛОВОЗРЕЛЫХ КРЫС В УСЛОВИЯХ ВОЗДЕЙСТВИЯ НА ОРГАНИЗМ СУЛЬФАТОВ МЕДИ, ЦИНКА И ЖЕЛЕЗА - С целью изучения масометрических показателей крыс и их головного мозга в условиях длительного действия (в течение 90 суток) на организм сульфатов меди, цинка и железа был проведен эксперимент на 48 белых половозрелых крысах-самцах массой 200250 г в возрасте 5-7 месяцев. Применялись анатомические, статистические и общепринятые методики микроанатомического метода исследования. Установлено, что комбинированное воздействие на организм сульфатов меди и цинка и железа оказывает на мозг достаточно выразительный токсический эффект, что отрицательно сказывается на массометрических показателях общего веса крыс и веса головного мозга. Это свидетельствует о развитии в головном мозге явлений острого отека с признаками геморрагической инфильтрации, степень выраженности которого максимальна в конце эксперимента.<br />FEATURES OF MASS INDICES AND MORPHOLOGICAL CHANGES IN ADULT RAT BRAIN UNDER THE INFLUENCE ON THE BODY OF COPPER SULFATE, ZINC AND IRON - To study the performance of rats and their mass brain in long acting (for 90 days) on the body of copper sulfate, zinc and iron, an experiment was conducted on 48 white adult male rats weighing 200-250 gram, aged 5-7 months. There was applied anatomy, statistics and conventional techniques microanatomical research method. It was established that the combined effect on the body of copper and zinc sulphates and iron in the brain has enough expressive toxicity, which affects performance on the total weight of the rats and brain weight. This testifies to the development of brain edema, acute phenomena with signs of hemorrhagic infiltration. The severity of edema increases and reaches maximum performance at the end of the experiment.<br />Ключові слова: головний мозок, солі важких металів, відносна маса, коефіцієнт цефалізації.<br />Ключевые слова: головной мозг, соли тяжелых металлов, относительная масса, коэффициент цефа- лизации.<br />Key words: brain, salts of heavy metals, relative mass, ratio cephalization.

Essential role of oligodendrocytes in the formation and maintenance of central nervous system nodal regions

Development ◽  
2001 ◽  
Vol 128 (23) ◽  
pp. 4881-4890 ◽  
Author(s):  
Carole Mathis ◽  
Natalia Denisenko-Nehrbass ◽  
Jean-Antoine Girault ◽  
Emiliana Borrelli
Keyword(s):  
Na Channels ◽  
Myelinated Axons ◽  
K Channels ◽  
Protein Levels ◽  
Ankyrin G ◽  
Specific Proteins ◽  
Jimpy Mice ◽  
The Brain

The membrane of myelinated axons is divided into functionally distinct domains characterized by the enrichment of specific proteins. The mechanisms responsible for this organization have not been fully identified. To further address the role of oligodendrocytes in the functional segmentation of the axolemma in vivo, the distribution of nodal (Na+ channels, ankyrin G), paranodal (paranodin/contactin-associated-protein) and juxtaparanodal (Kv1.1 K+ channels) axonal markers, was studied in the brain of MBP-TK and jimpy mice. In MBP-TK transgenic mice, oligodendrocyte ablation was selectively induced by FIAU treatment before and during the onset of myelination. In jimpy mice, oligodendrocytes degenerate spontaneously within the first postnatal weeks after the onset of myelination. Interestingly, in MBP-TK mice treated for 1-20 days with FIAU, despite the ablation of more than 95% of oligodendrocytes, the protein levels of all tested nodal markers was unaltered. Nevertheless, these proteins failed to cluster in the nodal regions. By contrast, in jimpy mice, despite a diffused localization of paranodin, the formation of nodal clusters of Na+ channels and ankyrin G was observed. Furthermore, K+ channels clusters were transiently visible, but were in direct contact with nodal markers. These results demonstrate that the organization of functional domains in myelinated axons is oligodendrocyte dependent. They also show that the presence of these cells is a requirement for the maintenance of nodal and paranodal regions.

scholarly journals The Effect of the APOE4 Gene on Accumulation of Aβ 40 After Brain Injury Cannot Be Reversed by Increasing apoE4 Protein

2016 ◽  
Vol 75 (8) ◽  
pp. 770-778 ◽  
Author(s):  
Patricia M. Washington ◽  
Mark P. Burns
Keyword(s):  
Brain Injury ◽  
Amyloid Precursor Protein Processing ◽  
Biphasic Response ◽  
Protein Levels ◽  
Abnormal Accumulation ◽  
Apoe Protein ◽  
Rapid Clearance ◽  
Amyloid Aβ ◽  
Β Amyloid ◽  
The Brain

Abstract The apolipoprotein E (apoE) protein is involved in clearance of β-amyloid (Aβ) from the brain; and the APOE4 gene is associated with Aβ plaque formation in humans following traumatic brain injury (TBI). Here, we examined the association between apoE and Aβ 40 after experimental TBI and the effects of APOE alleles on this relationship. We report a biphasic response of soluble apoE protein after TBI with an acute reduction at 1 day postinjury followed by an increase at 7 days postinjury. TBI-induced Aβ 40 levels decreased as soluble apoE levels increased. In APOE4 mice there was a diminished apoE response to TBI that corresponded to prolonged accumulation of TBI-induced Aβ 40 versus that in APOE3 mice. Amyloid precursor protein processing was similar in APOE3 and APOE4 mice suggesting that impaired clearance was responsible for the abnormal accumulation of Aβ 40 in the latter. Treatment of APOE4 mice with bexarotene for 7 days increased apoE4 protein levels but was not sufficient to reduce TBI-induced Aβ 40 . Thus, rapid clearance of TBI-induced Aβ 40 occurs in mice but these pathways are impaired in APOE4 carriers. These data may help explain the deposition of Aβ in APOE4 carriers and the increased incidence of brain Aβ plaques following TBI.

scholarly journals Fractalkine Attenuates Microglial Cell Activation Induced by Prenatal Stress

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Joanna Ślusarczyk ◽  
Ewa Trojan ◽  
Katarzyna Głombik ◽  
Katarzyna Chamera ◽  
Adam Roman ◽  
...  
Keyword(s):  
Prenatal Stress ◽  
Cell Activation ◽  
Inflammatory Factors ◽  
Potential Contribution ◽  
Fractalkine Receptor ◽  
Neuropsychiatric Diseases ◽  
Prenatally Stressed ◽  
The Brain ◽  
Receptor Cx3cr1

The potential contribution of inflammation to the development of neuropsychiatric diseases has recently received substantial attention. In the brain, the main immune cells are the microglia. As they are the main source of inflammatory factors, it is plausible that the regulation of their activation may be a potential therapeutic target. Fractalkine (CX3CL1) and its receptor CX3CR1 play a crucial role in the control of the biological activity of the microglia. In the present study, using microglial cultures we investigated whether fractalkine is able to reverse changes in microglia caused by a prenatal stress procedure. Our study found that the microglia do not express fractalkine. Prenatal stress decreases the expression of the fractalkine receptor, which in turn is enhanced by the administration of exogenous fractalkine. Moreover, treatment with fractalkine diminishes the prenatal stress-induced overproduction of proinflammatory factors such as IL-1β, IL-18, IL-6, TNF-α, CCL2, or NO in the microglial cells derived from prenatally stressed newborns. In conclusion, the present results revealed that the pathological activation of microglia in prenatally stressed newborns may be attenuated by fractalkine administration. Therefore, understanding of the role of the CX3CL1-CX3CR1 system may help to elucidate the mechanisms underlying the neuron-microglia interaction and its role in pathological conditions in the brain.

scholarly journals Epigenetic mechanism of carbohydrate sulfotransferase 3 (CHST3) downregulation in the aging brain

2019 ◽  
Author(s):  
David Baidoe-Ansah ◽  
M Sadman Sakib ◽  
Shaobo Jia ◽  
Andre Fischer ◽  
Rahul Kaushik ◽  
...  
Keyword(s):  
Chondroitin Sulfate ◽  
Brain Plasticity ◽  
Epigenetic Mechanism ◽  
Aging Brain ◽  
Chondroitin Sulfates ◽  
Expression Of Genes ◽  
Bona Fide ◽  
Old Mice ◽  
The Brain

AbstractNeural extracellular matrix (ECM) is a complex molecular meshwork surrounding neurons and glial cells in the extracellular space. Structural and functional state of ECM in the brain is tightly regulated by various components of neural ECM such as hyaluronic acid, chondroitin sulfate proteoglycans, link proteins, tenascins, various matrix-modifying enzymes such as chondroitin sulfate synthases and carbohydrate sulfotransferase together with matrix-degrading enzymes. Age-dependent accumulation of ECM molecules is implicated in the age-associated decline in synaptic and cognitive functions. Understanding age-associated changes in the expression of genes involved in regulating various components of ECM can provide an insight into the role of ECM in the aging brain. Hence, in this study, we compared the expression levels of ECM regulating genes in three groups of mice: 2-3 months old mice (2-3M), 22- to 26-month-old mice (22-26M) and more than 30-month-old mice (>30M). Using qPCR, we discovered that in the hippocampus of >30M old mice, the majority of ECM related genes are downregulated, while genes related to neuroinflammation are highly upregulated. This pattern was accompanied by a decrease in cognitive performance of the >30M old mice and was most correlated among ECM-related genes with the downregulation of carbohydrate sulfotransferase 3 (CHST3) gene expression. Interestingly, in 24-26M mice, no general decrease in the expression of ECM related genes was observed, although we still found the upregulation in neuroinflammatory genes and downregulation of CHST3. Further analysis of epigenetic mechanisms revealed a decrease in H3K4me3, three methyl groups at the lysine 4 on the histone H3 proteins, associated with the promoter region of CHST3 gene in non-neuronal (NeuN-negative) but not in neuronal (NeuN-positive) cells. We conclude that in 22-26 M old brains there are minor changes in expression of the studied bona fide neural ECM genes but there is a prominent epigenetic dysregulation of the CHST3 gene responsible for 6-sulfation of chondroitin sulfates, which may lead to impaired brain plasticity and cognitive decline.

scholarly journals The Presence and Potential Role of ALDH1A2 in the Glioblastoma Microenvironment

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2485
Author(s):  
Stephanie Sanders ◽  
Denise M. Herpai ◽  
Analiz Rodriguez ◽  
Yue Huang ◽  
Jeff Chou ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Potential Role ◽  
Therapeutic Agents ◽  
Brain Parenchyma ◽  
Low Grade ◽  
Effective Management ◽  
Diffuse Infiltration ◽  
Protein Levels ◽  
The Brain

Glioblastoma (GBM) is the most aggressive malignant glioma. Therapeutic targeting of GBM is made more difficult due to its heterogeneity, resistance to treatment, and diffuse infiltration into the brain parenchyma. Better understanding of the tumor microenvironment should aid in finding more effective management of GBM. GBM-associated macrophages (GAM) comprise up to 30% of the GBM microenvironment. Therefore, exploration of GAM activity/function and their specific markers are important for developing new therapeutic agents. In this study, we identified and evaluated the expression of ALDH1A2 in the GBM microenvironment, and especially in M2 GAM, though it is also expressed in reactive astrocytes and multinucleated tumor cells. We demonstrated that M2 GAM highly express ALDH1A2 when compared to other ALDH1 family proteins. Additionally, GBM samples showed higher expression of ALDH1A2 when compared to low-grade gliomas (LGG), and this expression was increased upon tumor recurrence both at the gene and protein levels. We demonstrated that the enzymatic product of ALDH1A2, retinoic acid (RA), modulated the expression and activity of MMP-2 and MMP-9 in macrophages, but not in GBM tumor cells. Thus, the expression of ALDH1A2 may promote the progressive phenotype of GBM.

scholarly journals The Role of the Adipokines in the Most Common Gestational Complications

2020 ◽  
Vol 21 (24) ◽  
pp. 9408
Author(s):  
Paweł Gutaj ◽  
Rafał Sibiak ◽  
Maurycy Jankowski ◽  
Karina Awdi ◽  
Rut Bryl ◽  
...  
Keyword(s):  
Experimental Studies ◽  
Diagnostic Value ◽  
Potential Contribution ◽  
Protein Levels ◽  
Standard Clinical Practice ◽  
Early Markers ◽  
Exact Etiology ◽  
Molecular Pathophysiology ◽  
Growth Abnormalities

Adipocytokines are hormonally active molecules that are believed to play a key role in the regulation of crucial biological processes in the human body. Numerous experimental studies established significant alterations in the adipokine secretion patterns throughout pregnancy. The exact etiology of various gestational complications, such as gestational diabetes, preeclampsia, and fetal growth abnormalities, needs to be fully elucidated. The discovery of adipokines raised questions about their potential contribution to the molecular pathophysiology of those diseases. Multiple studies analyzed their local mRNA expression and circulating protein levels. However, most studies report conflicting results. Several adipokines such as leptin, resistin, irisin, apelin, chemerin, and omentin were proposed as potential novel early markers of heterogeneous gestational complications. The inclusion of the adipokines in the standard predictive multifactorial models could improve their prognostic values. Nonetheless, their independent diagnostic value is mostly insufficient to be implemented into standard clinical practice. Routine assessments of adipokine levels during pregnancy are not recommended in the management of both normal and complicated pregnancies. Based on the animal models (e.g., apelin and its receptors in the rodent preeclampsia models), future implementation of adipokines and their receptors as new therapeutic targets appears promising but requires further validation in humans.

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