scholarly journals Ischemic Neuronal Injury is Ameliorated by Astrocyte Activation

1998 ◽  
Vol 25 (2) ◽  
pp. 102-107 ◽  
Author(s):  
Deon F. Louw ◽  
Tetsuy Masada ◽  
Garnette R. Sutherland
Keyword(s):  
Ethidium Bromide ◽  
Neuronal Injury ◽  
Contralateral Side ◽  
Forebrain Ischemia ◽  
Astrocyte Activation ◽  
Hippocampal Ca1 ◽  
Hippocampal Ca1 Sector ◽  
Ischemic Neuronal Injury

ABSTRACT:Background:The motivation of this study was to more precisely define the in vivo role of astrocytes in forebrain ischemia. Controversy exists in the literature as to whether they protect or injure neurons in this setting.Methods:Astrocytes in the rat hippocampus were disabled with stereotactic administration of a gliotoxin, ethidium bromide, 3 days prior to induction of forebrain ischemia. The extent of neuronal injury in this group was compared to a control category receiving intrahippocampal saline only.Results:Saline-injected animals demonstrated decreased hippocampal CA1 sector injury, and increased gliosis on the side of the injection compared to the contralateral side (P < 0.01) or ethidium bromide-treated animals (P < 0.05).Conclusion:The results suggest that activated astrocytes are protective to neurons subjected to an ischemic insult. This may result from their ability to elaborate neurotrophic factors, buffer potassium and metabolize a variety of neurotransmitters.

scholarly journals Involvement of HECTD1 in LPS-induced astrocyte activation via σ-1R-JNK/p38-FOXJ2 axis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ying Tang ◽  
Mengchun Zhou ◽  
Rongrong Huang ◽  
Ling Shen ◽  
Li Yang ◽  
...  
Keyword(s):  
Inflammatory Responses ◽  
Astrocyte Activation ◽  
Hect Domain ◽  
P38 Inhibitor ◽  
Ubiquitin Protein Ligase ◽  
Primary Mouse ◽  
Lps Treatment

Abstract Background Astrocytes participate in innate inflammatory responses within the mammalian central nervous system (CNS). HECT domain E3 ubiquitin protein ligase 1 (HECTD1) functions during microglial activation, suggesting a connection with neuroinflammation. However, the potential role of HECTD1 in astrocytes remains largely unknown. Results Here, we demonstrated that HECTD1 was upregulated in primary mouse astrocytes after 100 ng/ml lipopolysaccharide (LPS) treatment. Genetic knockdown of HECTD1 in vitro or astrocyte-specific knockdown of HECTD1 in vivo suppressed LPS-induced astrocyte activation, whereas overexpression of HECTD1 in vitro facilitated LPS-induced astrocyte activation. Mechanistically, we established that LPS activated σ-1R-JNK/p38 pathway, and σ-1R antagonist BD1047, JNK inhibitor SP600125, or p38 inhibitor SB203580 reversed LPS-induced expression of HECTD1, thus restored LPS-induced astrocyte activation. In addition, FOXJ2 functioned as a transcription factor of HECTD1, and pretreatment of primary mouse astrocytes with BD1047, SB203580, and SP600125 significantly inhibited LPS-mediated translocation of FOXJ2 into the nucleus. Conclusions Overall, our present findings suggest that HECTD1 participates in LPS-induced astrocyte activation by activation of σ-1R-JNK/p38-FOXJ2 pathway and provide a potential therapeutic strategy for neuroinflammation induced by LPS or any other neuroinflammatory disorders.

scholarly journals POS1388 ULTRASOUND FOR PANNICULITIS

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 977.1-977
Author(s):  
A. Potapova ◽  
O. Egorova ◽  
O. Alekseeva ◽  
A. Volkov ◽  
S. Radenska-Lopovok
Keyword(s):  
Dynamic Range ◽  
Subcutaneous Fat ◽  
Diagnostic Value ◽  
High Energy ◽  
Contralateral Side ◽  
Imaging Method ◽  
Non Invasive ◽  
M 12

Background:Ultrasound (US) is a non-invasive and safe imaging method that allows in vivo differentiation of the morphological structures of subcutaneous fat (SCF) tissue in in normal and pathology.Objectives:Reveal features of ultrasound changes in SCF in panniculitis (Pn).Methods:57 patients (f – 45, m - 12) aged 18 - 67 years with an initial diagnosis of erythema nodosum and a disease duration of 3.6 ± 1.4 years were examined. In addition to the general clinical examination, a computed tomography of the chest organs and a pathomorphological examination of a skin biopsy from the site of the node were performed. Ultrasound was performed on a MyLabTwice apparatus (ESAOTE, Italy) using a multi-frequency linear transducer (10-18 MHz) with the PD technique, the parameters of which were adapted for recording low-speed flows (PRF 300-600 Hz, low filter, dynamic range - 20-40 dB), the presence of vascularization was assessed not only in the affected area, but also on the contralateral side using high-energy Doppler.Results:33 patients were diagnosed with septal Pn (SPn), 24 - lobular Pn (LPn). In all cases, the diagnosis was verified by histological examination. Ultrasound made it possible to assess the thickness, echoicity and vascularization of the SCF. In 35 patients, significant thickening of the SCF was revealed (as compared to the contralateral side), of which in 14 cases with SPn, in 21 - with LPn. Significant diffuse thickening of the SCF with the contralateral side was observed in 18 patients, incl. in 12 (66%) patients with LPn. Limited thickening was more typical for SPn (73%). A significant increase in the echoicity of the SCF was noted in all forms of Pn. A “lobular” echo pattern with an anechogenic environment was observed in 25 patients, of which 18 (72%) had LPn. An increase in vascularization compared to the contralateral side was recorded in 30 cases (SPn-17, LPn-13).Conclusion:The obtained preliminary results indicate the important role of ultrasound in assessing the depth and prevalence of the inflammatory process at Pn. To clarify the diagnostic value of this method, further studies are needed on a larger sample of patients.Disclosure of Interests:None declared

Role of extracellular RNA in neuronal injury-induced astrocyte activation

2011 ◽  
Vol 71 ◽  
pp. e329
Author(s):  
Tatsuya Kibayashi ◽  
Takahiro Katayama ◽  
Hiroki Tanaka ◽  
Hikaru Igarashi ◽  
Yuuki Yamashita ◽  
...  
Keyword(s):  
Neuronal Injury ◽  
Astrocyte Activation ◽  
Extracellular Rna

scholarly journals Epidermal Growth Factor Protects Neuronal Cells In Vivo and In Vitro against Transient Forebrain Ischemia- and Free Radical-Induced Injuries

1998 ◽  
Vol 18 (4) ◽  
pp. 349-360 ◽  
Author(s):  
Hui Peng ◽  
Tong-Chun Wen ◽  
Junya Tanaka ◽  
Nobuji Maeda ◽  
Seiji Matsuda ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cultured Neurons ◽  
Forebrain Ischemia ◽  
Hippocampal Ca1 ◽  
Epidermal Growth

Epidermal growth factor (EGF) has been considered to be a candidate for neurotrophic factors on the basis of the results of several in vitro studies. However, the in vivo effect of EGF on ischemic neurons as well as its mechanism of action have not been fully understood. In the present in vivo study using a gerbil ischemia model, we examined the effects of EGF on ischemia-induced learning disability and hippocampal CA1 neuron damage. Cerebroventricular infusion of EGF (24 or 120 ng/d) for 7 days to gerbils starting 2 hours before or immediately after transient forebrain ischemia caused a significant prolongation of response latency time in a passive avoidance task in comparison with the response latency of vehicle-treated ischemic animals. Subsequent histologic examinations showed that EGF effectively prevented delayed neuronal death of CA1 neurons in the stratum pyramidale and preserved synapses intact within the strata moleculare, radiatum, and oriens of the hippocampal CA1 region. In situ detection of DNA fragmentation (TUNEL staining) revealed that ischemic animals infused with EGF contained fewer TUNEL-positive neurons in the hippocampal CA1 field than those infused with vehicle alone at the seventh day after ischemia. In primary hippocampal cultures, EGF (0.048 to 6.0 ng/mL) extended the survival of cultured neurons, facilitated neurite outgrowth, and prevented neuronal damage caused by the hydroxyl radical-producing agent FeSO4 and by the peroxynitrite-producing agent 3-morpholinosydnonimine in a dose-dependent manner. Moreover, EGF significantly attenuated FeSO4-induced lipid peroxidation of cultured neurons. These findings suggest that EGF has a neuroprotective effect on ischemic hippocampal neurons in vivo possibly through inhibition of free radical neurotoxicity and lipid peroxidation.

scholarly journals The Role of SUMO-Conjugating Enzyme Ubc9 in the Neuroprotection of Isoflurane Preconditioning Against Ischemic Neuronal Injury

2014 ◽  
Vol 51 (3) ◽  
pp. 1221-1231 ◽  
Author(s):  
Li Tong ◽  
Zhixin Wu ◽  
Mingzi Ran ◽  
Yu Chen ◽  
Lujia Yang ◽  
...  
Keyword(s):  
Neuronal Injury ◽  
Ischemic Neuronal Injury ◽  
Conjugating Enzyme

scholarly journals Critical Role of Calpain I in Mitochondrial Release of Apoptosis-Inducing Factor in Ischemic Neuronal Injury

2007 ◽  
Vol 27 (35) ◽  
pp. 9278-9293 ◽  
Author(s):  
G. Cao ◽  
J. Xing ◽  
X. Xiao ◽  
A. K. F. Liou ◽  
Y. Gao ◽  
...  
Keyword(s):  
Critical Role ◽  
Neuronal Injury ◽  
Apoptosis Inducing Factor ◽  
Ischemic Neuronal Injury

scholarly journals Dexamethasone Aggravates Ischemia-Induced Neuronal Damage by Facilitating the Onset of Anoxic Depolarization and the Increase in the Intracellular Ca2+ Concentration in Gerbil Hippocampus

1998 ◽  
Vol 18 (3) ◽  
pp. 274-280 ◽  
Author(s):  
Naoto Adachi ◽  
Junfeng Chen ◽  
Keyue Liu ◽  
Shinzo Tsubota ◽  
Tatsuru Arai
Keyword(s):  
Direct Current ◽  
Neuronal Damage ◽  
Induced Membrane ◽  
Potential Shift ◽  
Hippocampal Ca1 ◽  
Intracellular Ca ◽  
Current Potential ◽  
Ischemic Neuronal Injury

The Ca2+ mobilization across the neuronal membrane is regarded as a crucial factor in the development of neuronal damage in ischemia. Because glucocorticoids have been reported to aggravate ischemic neuronal injury, the effects of dexamethasone on ischemia-induced membrane depolarization, histologic outcome, and changes in the intracellular Ca2+ concentration in the gerbil hippocampus were examined in vivo and in vitro. The effects of metyrapone, an inhibitor of glucocorticoid synthesis, were also evaluated. Changes in the direct-current potential shift in the hippocampal CA1 area produced by transient forebrain ischemia for 2.5 minutes were compared among animals pretreated with dexamethasone (3 μg, intracerebroventricularly), metyrapone (100 mg/kg, intraperitoneally), and saline. The histologic outcome was evaluated 7 days after ischemia by assessing the delayed neuronal death in the hippocampal CA1 pyramidal cells of these animals. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effect of dexamethasone (120 μg/L in the medium) on the cytosolic Ca2+ accumulation was examined. The effect in a Ca2+-free ischemialike condition was also investigated. Preischemic administration of dexamethasone reduced the onset latency of ischemia-induced membrane depolarization by 22%, and aggravated neuronal damage in vivo. In contrast, pretreatment with metyrapone improved the histologic outcome. The onset time of the increase in the intracellular concentration of Ca2+ provoked by in vitro hypoxia was advanced in dexamethasone-treated slices. The Ca2+-free in vitro hypoxia reduced the elevation compared with that in the Ca2+-containing condition. Treatment with dexamethasone facilitated the increase on both the initiation and the extent in the Ca2+-free condition. Aggravation of ischemic neuronal injury by endogenous or exogenous glucocorticoids is thus thought to be caused by the advanced onset times of both the ischemia-induced direct-current potential shift and the increase in the intracellular Ca2+ concentration.

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