scholarly journals Are Temporal Differences in GDNF and NOS Isoform Induction Contributors to Neurodegeneration? A Fluorescence Microscopy-Based Study

2016 ◽  
Vol 10 (1) ◽  
pp. 67-76 ◽  
Author(s):  
Marie-Francoise Doursout ◽  
Yangyan Liang ◽  
Mya C. Schiess ◽  
Angelica Padilla ◽  
Brian J. Poindexter ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Glial Cell ◽  
Cell Activation ◽  
Immune Cell ◽  
Serum Levels ◽  
Protective Effects ◽  
Glial Cell Activation ◽  
Inflammatory Stimuli ◽  
Rescue Agent ◽  
Oxide Synthase

Background:Specific factors in Parkinson’s disease have become targets as to their protective and degenerative effects. We have demonstrated that cytokines and PD-CSF detrimentally affect microglia and astrocyte growth. While glial cell-derived neurotrophic factor (GDNF) has been recognized as a possible neuron-rescue agent, nitric oxide synthase (NOS) has been implicated in neurodegenerative processes.Objective:To demonstrate that glial cell activation, cytokine production, and NOS induction, play an intimate role in the loss of dopaminergic signaling,viamechanisms that are a result of inflammation and inflammatory stimuli.Methods:Study animals were sacrificed following endotoxin treatment and tissue sections were harvested and probed for GDNF and NOS isomers by fluorescence deconvolution microscopy. Fluorescence was mapped and quantified for each probeResults:An immune cell influx into ‘vulnerable’ areas of the brain was seen, and three NOS isomers, inducible (iNOS), neuronal (nNOS) and endothelial (eNOS), were synthesized in the brains, a finding which suggests that each isomer has a role in neurodegeneration. eNOS was found associated with blood vessels, while iNOS was associated with glial and matrix cells and nNOS was located with both glia and neurons. Following endotoxin treatment, serum levels of nitric oxide were higher at 6-8 hours, while tissue levels of NOS were elevated for much longer. Thus, induction of NOS occurred earlier than the induction of GDNF.Conclusion:Our findings suggest that the protective abilities of GDNF to combat neural destruction are not available rapidly enough, and do not remain at sufficiently high levels long enough to assert its protective effects. (250).

Abstract 5293: A New Animal Model of Hypercholesterolemia and Atherosclerosis: Mice Deficient in All Nitric Oxide Synthases

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Masato Tsutsui ◽  
Yasuko Yatera ◽  
Hiroaki Shimokawa ◽  
Sei Nakata ◽  
Kiyoko Shibata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Low Density Lipoprotein ◽  
Atherosclerotic Lesion ◽  
Density Lipoprotein ◽  
Serum Levels ◽  
Vascular Lesion ◽  
Lesion Formation ◽  
Regular Diet ◽  
Oxide Synthase ◽  
Nos Isoforms

We have recently developed mice lacking all three nitric oxide synthase (NOS) isoforms: nNOS, iNOS, and eNOS ( PNAS 2005). In this study, we examined the effects of a high-cholesterol (HC) diet on lipid metabolism and vascular lesion formation in those mice. Experiments were performed in 2-month-old male wild-type (WT) and singly, doubly, and triply NOS −/− mice (n=6–9). They were maintained on either a regular diet or a HC diet for 3 months. The HC feeding significantly increased plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL) in all the genotypes studied as compared on the regular diet (all P <0.05). These serum levels of TC and LDL on the HC diet (mg/dl) were both significantly higher in all the singly, doubly, and triply NOS −/− genotypes as compared with the WT genotype (singly nNOS −/− [371±61 and 205±65], iNOS −/− [559±62 and 350±62], eNOS −/− [619±22 and 395±25], doubly n/iNOS −/− [518±77 and 328±72], n/eNOS −/− [635±56 and 458.8±42], e/iNOS −/− [480±38 and 260±40], triply n/i/eNOS −/− [2316±704 and 1588±715], and WT [326±43 and 244±54]) (all P <0.05). Notably, the extent of the dyslipidemia was by far severest in the triply n/i/eNOS −/− genotype among the NOS −/− genotypes, and intriguingly, the serum levels of TC and LDL in the triply n/i/eNOS −/− genotype were equivalent to those in apolipoprotein E −/− mice that exhibit severe hypercholesterolemia. Lipid accumulation in the aorta on the HC diet (lipid area, %, oil red O staining) was also significantly more accelerated in all the NOS −/− genotypes than in the WT genotype (singly nNOS −/− [6.6±1.5], iNOS −/− [6.7±2.2], eNOS −/− [5.5±2.3], doubly n/iNOS −/− [4.7±1.7], n/eNOS −/− [6.4±1.4], i/eNOS −/− [6.8±1.3], triply n/i/eNOS −/− [20.6±1.0], and WT [3.6±1.2]), while the extent of the aortic atherosclerosis was again by far severest in the triply n/i/eNOS −/− genotype (all P <0.05). These results demonstrate that mice deficient in all NOSs manifest severe hypercholesterolemia and lipid-rich atherosclerotic lesion formation in response to a HC diet, indicating a pivotal role of the whole NOS system in preventing those disorders. Our triply NOS −/− mouse is a new experimental model of human hypercholesterolemia and atherosclerosis.

Toll-like receptor 2 contributes to glial cell activation and heme oxygenase-1 expression in traumatic brain injury

2008 ◽  
Vol 431 (2) ◽  
pp. 123-128 ◽  
Author(s):  
Chanhee Park ◽  
Ik-Hyun Cho ◽  
Donghoon Kim ◽  
Eun-Kyeong Jo ◽  
Se-Young Choi ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glial Cell ◽  
Heme Oxygenase ◽  
Cell Activation ◽  
Heme Oxygenase 1 ◽  
Toll Like Receptor ◽  
Glial Cell Activation ◽  
Toll Like Receptor 2

scholarly journals Neuroinflammation and glial cell activation in mental disorders

2020 ◽  
Vol 2 ◽  
pp. 100034 ◽  
Author(s):  
Priscila G.C. Almeida ◽  
João Victor Nani ◽  
Jean Pierre Oses ◽  
Elisa Brietzke ◽  
Mirian A.F. Hayashi
Keyword(s):  
Mental Disorders ◽  
Glial Cell ◽  
Cell Activation ◽  
Glial Cell Activation

scholarly journals Effects of short chain alkanols on the inducible nitric oxide synthase in a glial cell line

1999 ◽  
Vol 126 (5) ◽  
pp. 1253-1261 ◽  
Author(s):  
Peter J Syapin ◽  
Alexia Rendon ◽  
David R Huron ◽  
Julius D Militante
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cell Line ◽  
Glial Cell ◽  
Inducible Nitric Oxide Synthase ◽  
Short Chain ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Protective Effect of Ocotillol, the Derivate of Ocotillol-Type Saponins in Panax Genus, against Acetic Acid-Induced Gastric Ulcer in Rats Based on Untargeted Metabolomics

2020 ◽  
Vol 21 (7) ◽  
pp. 2577 ◽  
Author(s):  
Cuizhu Wang ◽  
Yuze Yuan ◽  
He Pan ◽  
Alan Chen-Yu Hsu ◽  
Jinluan Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acetic Acid ◽  
Gastric Ulcer ◽  
Growth Factor ◽  
Gastric Mucosa ◽  
Epidermal Growth Factor ◽  
Serum Levels ◽  
Gastroprotective Effect ◽  
Epidermal Growth ◽  
Oxide Synthase

Gastric ulcer (GU), a prevalent digestive disease, has a high incidence and is seriously harmful to human health. Finding a natural drug with a gastroprotective effect is needed. Ocotillol, the derivate of ocotillol-type saponins in the Panax genus, possesses good anti-inflammatory activity. The study aimed to investigate the gastroprotective effect of ocotillol on acetic acid-induced GU rats. The serum levels of endothelin-1 (ET-1) and nitric oxide (NO), the gastric mucosa levels of epidermal growth factor, superoxide dismutase and NO were assessed. Hematoxylin and eosin staining of gastric mucosa for pathological changes and immunohistochemical staining of ET-1, epidermal growth factor receptors and inducible nitric oxide synthase were evaluated. A UPLC-QTOF-MS-based serum metabolomics approach was applied to explore the latent mechanism. A total of 21 potential metabolites involved in 7 metabolic pathways were identified. The study helps us to understand the pathogenesis of GU and to provide a potential natural anti-ulcer agent.

scholarly journals Activation of σ1 and σ2 receptors by afobazole increases glial cell survival and prevents glial cell activation and nitrosative stress after ischemic stroke

2016 ◽  
Vol 139 (3) ◽  
pp. 497-509 ◽  
Author(s):  
Christopher Katnik ◽  
Angela Garcia ◽  
Adam A. Behensky ◽  
Ilya E. Yasny ◽  
Alex M. Shuster ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cell Survival ◽  
Glial Cell ◽  
Cell Activation ◽  
Nitrosative Stress ◽  
Glial Cell Activation
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