JNK/Elk1 signaling and PCNA protein expression in the brain of hibernating frog Pelophylax esculentus

2021 ◽  
Author(s):  
Sara Falvo ◽  
Alessandra Santillo ◽  
Maria Maddalena Di Fiore ◽  
Luigi Rosati ◽  
Gabriella Chieffi Baccari
Keyword(s):  
Protein Expression ◽  
Pelophylax Esculentus ◽  
The Brain

Abstract P059: A A Role of Aminopeptidase A in the Brain on Cardiovascular Regulation of Conscious Rat

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Takuto Nakamura ◽  
Masanobu Yamazato ◽  
Akio Ishida ◽  
Yusuke Ohya
Keyword(s):  
Blood Pressure ◽  
Protein Expression ◽  
Drinking Behavior ◽  
Cardiovascular Regulation ◽  
Ang Ii ◽  
Hypertensive Rats ◽  
Aminopeptidase A ◽  
The Brain

Objective: Aminopeptidase A (APA) have important role in conversion of Ang II to Ang III. Intravenous APA administration lowers blood pressure in hypertensive rats. In contrast, APA inhibition in the brain lowers blood pressure in hypertensive rats. Therefore APA might have different role on cardiovascular regulation. However, a role of APA and Ang III on cardiovascular regulation especially in the brain has not been fully understood. Our purpose of present study was to investigate a role of APA and Ang III in the brain on cardiovascular regulation in conscious state. Method: 12-13 weeks old Wistar Kyoto rat (WKY) and 12-16 weeks old spontaneously hypertensive rat (SHR) were used. i) APA distribution in the brain was evaluated by immunohistochemistry. Protein expression of APA was evaluated by Western blotting. Enzymatic activity of APA was evaluated using L-glutamic acid γ-(4-nitroanilide) as a substrate. ii) WKY received icv administration of Ang II 25ng/2μL and Ang III 25ng/2μL. We recorded change in mean arterial pressure (MAP) in conscious and unrestraied state and measured induced drinking time. iii) SHR received icv administeration of recombinant APA 400ng/4μL. We recorded change in MAP in conscious and unrestraied state and measured induced drinking time. Result: i) APA was diffusely immunostained in the cells of brain stem including cardiovascular regulatory area such as rostral ventrolateral medulla. Protein expression and APA activity in the brain were similar between WKY (n=3) and SHR (n=3).ii) Icv administration of Ang II increased MAP by 33.8±3.8 mmHg and induced drinking behavior for 405±90 seconds (n=4). Icv administration of Ang III also increased MAP by 24.7±2.4 mmHg and induced drinking behavior for 258±62 seconds (n=3). These vasopressor activity and induced drinking behavior was completely blocked by pretretment of angiotensin receptor type 1 blocker.iii) Icv administration of APA increased MAP by 10.0±1.7 mmHg (n=3). Conclusion: These results suggested that Ang III in the brain increase blood pressure by Angiotensin type 1 receptor dependent mechanism and APA in the brain may involved in blood pressure regulation as a vasopressor enzyme.

Expression of Zinc-Finger Antiviral Protein in hCMEC/D3 Human Cerebral Microvascular Endothelial Cells: Effect of a Toll-Like Receptor 3 Agonist

2021 ◽  
pp. 1-10
Author(s):  
Mako Okudera ◽  
Minami Odawara ◽  
Masashi Arakawa ◽  
Shogo Kawaguchi ◽  
Kazuhiko Seya ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Protein Expression ◽  
Zinc Finger ◽  
Microvascular Endothelial Cells ◽  
Brain Microvascular Endothelial Cells ◽  
Toll Like Receptor ◽  
Antiviral Protein ◽  
Polycytidylic Acid ◽  
Microvascular Endothelial ◽  
The Brain

<b><i>Introduction:</i></b> Invasion of viruses into the brain causes viral encephalitis, which can be fatal and causes permanent brain damage. The blood-brain barrier (BBB) protects the brain by excluding harmful substances and microbes. Brain microvascular endothelial cells are important components of the BBB; however, the mechanisms of antiviral reactions in these cells have not been fully elucidated. Zinc-finger antiviral protein (ZAP) is a molecule that restricts the infection of various viruses, and there are 2 major isoforms: ZAPL and ZAPS. Toll-like receptor 3 (TLR3), a pattern-recognition receptor against viral double-stranded RNA, is implicated in antiviral innate immune reactions. The aim of this study was to investigate the expression of ZAP in cultured hCMEC/D3 human brain microvascular endothelial cells treated with an authentic TLR3 agonist polyinosinic-polycytidylic acid (poly IC). <b><i>Methods:</i></b> hCMEC/D3 cells were cultured and treated with poly IC. Expression of ZAPL and ZAPS mRNA was investigated using quantitative reverse transcription-polymerase chain reaction, and protein expression of these molecules was examined using western blotting. The role of nuclear factor-κB (NF-κB) was examined using the NF-κB inhibitor, SN50. The roles of interferon (IFN)-β, IFN regulatory factor 3 (IRF3), tripartite motif protein 25 (TRIM25), and retinoic acid-inducible gene-I (RIG-I) in poly IC-induced ZAPS expression were examined using RNA interference. Propagation of Japanese encephalitis virus (JEV) was examined using a focus-forming assay. <b><i>Results:</i></b> ZAPS mRNA and protein expression was upregulated by poly IC, whereas the change of ZAPL mRNA and protein levels was minimal. Knockdown of IRF3 or TRIM25 decreased the poly IC-induced upregulation of ZAPS, whereas knockdown of IFN-β or RIG-I did not affect ZAPS upregulation. SN50 did not affect ZAPS expression. Knockdown of ZAP enhanced JEV propagation. <b><i>Conclusion:</i></b> ZAPL and ZAPS were expressed in hCMEC/D3 cells, and ZAPS expression was upregulated by poly IC. IRF3 and TRIM25 are involved in poly IC-induced upregulation of ZAPS. ZAP may contribute to antiviral reactions in brain microvascular endothelial cells and protect the brain from invading viruses such as JEV.

scholarly journals C60 Fullerene Prevents Restraint Stress-Induced Oxidative Disorders in Rat Tissues: Possible Involvement of the Nrf2/ARE-Antioxidant Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Olga O. Gonchar ◽  
Andriy V. Maznychenko ◽  
Nataliya V. Bulgakova ◽  
Inna V. Vereshchaka ◽  
Tomasz Tomiak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Protein Expression ◽  
Restraint Stress ◽  
Stress Condition ◽  
Rat Tissues ◽  
Stress Exposure ◽  
The Brain ◽  
Nrf2 Protein

The effects of C60FAS (50 and 500 μg/kg) supplementation, in a normal physiological state and after restraint stress exposure, on prooxidant/antioxidant balance in rat tissues were explored and compared with the effects of the known exogenous antioxidant N-acetylcysteine. Oxidative stress biomarkers (ROS, O2⋅−, H2O2, and lipid peroxidation) and indices of antioxidant status (MnSOD, catalase, GPx, GST, γ-GCL, GR activities, and GSH level) were measured in the brain and the heart. In addition, protein expression of Nrf2 in the nuclear and cytosol fractions as well as the protein level of antiradical enzyme MnSOD and GSH-related enzymes γ-GCLC, GPx, and GSTP as downstream targets of Nrf2 was evaluated by western blot analysis. Under a stress condition, C60FAS attenuates ROS generation and O2⋅− and H2O2 releases and thus decreases lipid peroxidation as well as increases rat tissue antioxidant capacity. We have shown that C60FAS supplementation has dose-dependent and tissue-specific effects. C60FAS strengthened the antiradical defense through the upregulation of MnSOD in brain cells and maintained MnSOD protein content at the control level in the myocardium. Moreover, C60FAS enhanced the GSH level and the activity/protein expression of GSH-related enzymes. Correlation of these changes with Nrf2 protein content suggests that under stress exposure, along with other mechanisms, the Nrf2/ARE-antioxidant pathway may be involved in regulation of glutathione homeostasis. In our study, in an in vivo model, when C60FAS (50 and 500 μg/kg) was applied alone, no significant changes in Nrf2 protein expression as well as in activity/protein levels of MnSOD and GSH-related enzymes in both tissues types were observed. All these facts allow us to assume that in the in vivo model, C60FAS affects on the brain and heart endogenous antioxidative statuses only during the oxidative stress condition.

c-fos protein expression in the brain of the anesthetized rat induced by colorectal distention

2001 ◽  
Vol 120 (5) ◽  
pp. A715-A716
Author(s):  
Helena F. Wizos ◽  
Melissa Guillaume ◽  
Ralph Norgren ◽  
Kathleen Smith ◽  
Loren A. Evey ◽  
...  
Keyword(s):  
Protein Expression ◽  
Fos Protein ◽  
Colorectal Distention ◽  
The Brain

CNS Inflammation Induced by Lipopolysaccharide Up-Regulates Hepatic Hepcidin Expression by Activating IL-6/JAK2/STAT3 Pathway in Mice

2020 ◽  
Author(s):  
fali zhang ◽  
peng zhao ◽  
zhongming Qian ◽  
mingkang zhong
Keyword(s):  
Protein Expression ◽  
Iron Metabolism ◽  
Serum Iron ◽  
Transferrin Saturation ◽  
Cns Inflammation ◽  
Inflammation Response ◽  
Stat3 Pathway ◽  
Hepcidin Expression ◽  
Mrna And Protein Expression ◽  
The Brain

Abstract BackgroundLPS triggers inflammation response in periphery, whether the infection in CNS induced by LPS ICV injection affected the peripheral iron metabolism was unknown , The current study was to find out whether LPS injected to the brain could regulate hepcidin expression in liver and peripheral iron metabolism. MethodsWide type mice (IL-6+/+) and IL-6-/- mice of 8-week-old were performed on ICV injection with LPS. After 6h, hepcidin expression in liver, as well as serum iron and transferrin saturation was detected and calculated, we also tested the IL-6/JAK2/STAT3 pathway in hepcidin regulation in liver of IL-6 knockout (IL-6-/- mice) and IL-6+/+ mice, AG490 as an inhibitor of JAK2 was used to confirm the effect of IL-6/JAK2/STAT3 pathway on hepcidin expression in liver. ResultsHepcidin mRNA, IL-6 mRNA and protein expression in the liver of IL-6-/- mice was significantly lower than IL-6+/+ mice after LPS administration. IL-6 deficiency abolished the decrease of serum iron, transferrin saturation induced by LPS injection. IL-6 deficiency also abolished the decrease of Fpn1, increase of pSTAT3 and Ft-L protein in liver. AG490 significantly reduced the pSTAT3 protein and abolished the changes of Fpn1 and Ft-L expression induced by LPS in liver. ConclusionThese finding provided further evidence that the effect of central inflammation on the hepatic hepcidin expression and peripheral iron metabolism.

scholarly journals Hemispherical asymmetry in reports gene or protein expression related to mood disorders in the brain of rodents: A pilot systematic review

IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S477
Author(s):  
Mauricio Schuler Nin ◽  
Felipe B. Almeida ◽  
Fernanda F.S. Da Silva ◽  
Alan R. Fonseca ◽  
Carina F. Feddern ◽  
...  
Keyword(s):  
Systematic Review ◽  
Protein Expression ◽  
Mood Disorders ◽  
The Brain

scholarly journals A Possible Link Between HCN Channels and Depression

2018 ◽  
Vol 2 ◽  
pp. 247054701878778 ◽  
Author(s):  
Chung Sub Kim ◽  
Daniel Johnston
Keyword(s):  
Protein Expression ◽  
Neuronal Excitability ◽  
Acute Stress ◽  
Hcn Channels ◽  
Chronic Unpredictable Stress ◽  
Ca1 Neurons ◽  
Ca1 Region ◽  
Hcn1 Channels ◽  
The Brain

Growing evidence suggests a possible link between hyperpolarization-activated cyclic nucleotide-gated nonselective cation (HCN) channels and depression. In a recent study published in Molecular Psychiatry, we first demonstrate that Ih (the membrane current mediated by HCN channels) and HCN1 protein expression were increased in dorsal, but not in ventral, CA1 region following chronic, but not acute stress. This upregulation of Ih was restricted to the perisomatic region of CA1 neurons and contributed to a reduction of neuronal excitability. A reduction of HCN1 protein expression in dorsal CA1 region before the onset of chronic unpredictable stress-induced depression was sufficient to provide resilient effects to chronic unpredictable stress. Furthermore, in vivo block of the sarcoplasmic/endoplasmic reticulum Ca2+-ATPase (SERCA) pumps, a manipulation known to increase intracellular calcium levels and upregulate Ih, produced anxiogenic-like behavior and an increase in Ih, similar to that observed in chronic unpredictable stress model of depression. Here, we share our view on (1) how the function and expression of HCN1 channels are changed in the brain in a subcellular region-specific manner during the development of depression and (2) how a reduction of HCN1 protein expression provides resilience to chronic stress.

scholarly journals Infection with Plasmodium berghei ookinetes alters protein expression in the brain of Anopheles albimanus mosquitoes

2016 ◽  
Vol 9 (1) ◽  
Author(s):  
Alejandro Alvarado-Delgado ◽  
Guillermo Perales Ortiz ◽  
Ángel T. Tello-López ◽  
Sergio Encarnación ◽  
Renaud Conde ◽  
...  
Keyword(s):  
Protein Expression ◽  
Plasmodium Berghei ◽  
Anopheles Albimanus ◽  
The Brain
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