Erythropoietin Downregulates Bax and DP5 ProApoptotic Gene Expression in Neonatal Hypoxic-Ischemic Brain Injury

Neonatology ◽  
2006 ◽  
Vol 89 (3) ◽  
pp. 205-210 ◽  
Author(s):  
Abdullah Kumral ◽  
Sermin Genc ◽  
Erdener Ozer ◽  
Osman Yilmaz ◽  
Necati Gokmen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Proapoptotic Gene

Abstract MP15: Hypoxia and Endothelin-1 in Microglial Cell Activation

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Francisco J Rodriguez-Matos ◽  
Sebastian O Castaño-Pesante ◽  
Jose R Romero ◽  
Yaritza Inostroza-Nieves
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Brain Injury ◽  
Cell Activation ◽  
Microglial Cell ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Endothelin 1 ◽  
Tnf Α ◽  
Hypoxic Ischemic Brain Injury

Oxidative stress and inflammatory responses play critical roles in hypoxic-ischemic brain injury. Microglial cells are rapidly activated in response to injury and stressful stimuli, including hypoxia. Endothelin-1 (ET-1) is a potent vasoconstrictor that has been associated with cerebrovascular diseases. Hypoxia stimulates endothelial ET-1 production. However, the role of ET-1 in microglia under hypoxia is not clear. The aim of this project was to characterize the effect of hypoxia in a human microglial cell line, HMC3. We induced hypoxia using a chamber (1% O2, 5% CO2, and 92 % N2) at 37 °C for 4h, 24h, and 48h. MUSE Oxidative Stress Assay was performed to measure reactive oxygen species (ROS) formation, ELISA to determine TNF, IL-6, and ET-1 levels, qPCR to measure gene expression of ET-1, and immunofluorescence staining to visualize and compare the presence of ET-1 in hypoxic and control group cells. It was observed that, when compared to normoxic HMC3 cells, hypoxic HMC3 exposure significantly increased the ROS by a factor of 2.5 (p<0.001, n=3), the pro-inflammatory cytokine TNF-α increased 3.8 times (p<0.01, n=4), and IL-6 increased by a factor of 1.6 (p<0.01, n=4). In addition, hypoxia stimulates ET-1 gene expression 5.0-fold (p<0.001, n=4) and increased protein production 1.3 times (p<0.01, n=4). Consequently, treatment with ET-1 increased the amount of ROS, TNF-α, and IL-6 in HMC3 cells by a factor of 1.4 (p<0.05, n=4), 1.6 (p<0.001, n=4), and 1.9 (p<0.05, n=4), respectively. All these events were blocked by ET-1 receptor A (ETRA) antagonist, BQ123. Our results suggest that hypoxic conditions create a cycle of microglial cell activation leading to increased ROS and ET-1 production that further stimulate microglial cells. Thus, we posit that the ET-1 receptor blockade represents a promising therapeutic approach to regulate microglial cell responses in hypoxic-ischemic brain injury.

Trace Fear Conditioning Detects Hypoxic-Ischemic Brain Injury in Neonatal Mice

2011 ◽  
Vol 33 (3-4) ◽  
pp. 222-230 ◽  
Author(s):  
Katarina Järlestedt ◽  
Alison L. Atkins ◽  
Henrik Hagberg ◽  
Marcela Pekna ◽  
Carina Mallard
Keyword(s):  
Brain Injury ◽  
Fear Conditioning ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Mice ◽  
Trace Fear Conditioning ◽  
Hypoxic Ischemic Brain Injury ◽  
Trace Fear

Minocycline: A neuroprotective agent for hypoxic-ischemic brain injury in the neonate?

2009 ◽  
Vol 87 (3) ◽  
pp. 599-608 ◽  
Author(s):  
Kathryn M. Buller ◽  
Michelle L. Carty ◽  
Hanna E. Reinebrant ◽  
Julie A. Wixey
Keyword(s):  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neuroprotective Agent ◽  
Hypoxic Ischemic Brain Injury

Focal protein synthesis inhibition in a model of neonatal hypoxic-ischemic brain injury

1987 ◽  
Vol 95 (2) ◽  
pp. 277-289 ◽  
Author(s):  
Barney E. Dwyer ◽  
Robert N. Nishimura ◽  
Clydette L. Powell ◽  
Susan L. Mailheau
Keyword(s):  
Protein Synthesis ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Protein Synthesis Inhibition ◽  
Ischemic Brain ◽  
Synthesis Inhibition ◽  
Hypoxic Ischemic Brain Injury
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