scholarly journals LED Induced Microglial Activation and Rise in Caspase3 Shows Reorganization in the Retina

2021 ◽  
Author(s):  
Boglárka Balogh ◽  
Gergely Szarka ◽  
Ádám J Tengölics ◽  
Gyula Hoffmann ◽  
Béla Völgyi ◽  
...  
Keyword(s):  
Microglial Activation ◽  
Caspase 3 ◽  
Light Exposure ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mrna Levels ◽  
Wide Spread ◽  
Light Emitting ◽  
Led Light ◽  
Retinal Tissue

Vision is our primary sense as the human eye is the gateway for more than 65% of information reaching the human brain. Today’s increased exposure to different wavelengths and intensities of light from Light Emitting Diodes (LEDs) sources could induce retinal degeneration and accompanying neuronal cell death. Damage induced by chronic phototoxic reactions occurring in the retina accumulates over years and it has been suggested to be responsible for the etiology of many debilitating ocular conditions. In this work, we examined how LED stimulation affects vision by monitoring changes in the expression of death and survival factors as well as microglial activation in LED-induced damage (LID) of the retinal tissue. We found an LED exposure-induced increase in the mRNA levels of major apoptosis-related markers -BAX, Bcl-2, and Caspase-3 and an accompanying wide-spread microglial and Caspase-3 activation. Everyday LED light exposure was accounted for all the described changes in the retinal tissue of mice in this study, indicating that overuse of non-filtered direct LED light can have detrimental effects on the human retina as well.

scholarly journals LED-Induced Microglial Activation and Rise in Caspase3 Suggest a Reorganization in the Retina

2021 ◽  
Vol 22 (19) ◽  
pp. 10418
Author(s):  
Boglárka Balogh ◽  
Gergely Szarka ◽  
Ádám J. Tengölics ◽  
Gyula Hoffmann ◽  
Béla Völgyi ◽  
...  
Keyword(s):  
Microglial Activation ◽  
Caspase 3 ◽  
Light Exposure ◽  
Light Emitting Diode ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Mrna Levels ◽  
Light Emitting ◽  
Led Light ◽  
Retinal Tissue

Vision is our primary sense as the human eye is the gateway for more than 65% of information reaching the human brain. Today’s increased exposure to different wavelengths and intensities of light from light emitting diode (LED) sources could induce retinal degeneration and accompanying neuronal cell death. Damage induced by chronic phototoxic reactions occurring in the retina accumulates over years and it has been suggested as being responsible for the etiology of many debilitating ocular conditions. In this work, we examined how LED stimulation affects vision by monitoring changes in the expression of death and survival factors as well as microglial activation in LED-induced damage (LID) of the retinal tissue. We found an LED-exposure-induced increase in the mRNA levels of major apoptosis-related markers BAX, Bcl-2, and Caspase-3 and accompanying widespread microglial and Caspase-3 activation. Everyday LED light exposure was accounted for in all the described changes in the retinal tissue of mice in this study, indicating that overuse of non-filtered direct LED light can have detrimental effects on the human retina as well.

scholarly journals Antarctic krill (Euphausia superba) exhibit positive phototaxis to white LED light

Polar Biology ◽  
2021 ◽  
Vol 44 (3) ◽  
pp. 483-489
Author(s):  
Bjørn A. Krafft ◽  
Ludvig A. Krag
Keyword(s):  
Antarctic Krill ◽  
Light Exposure ◽  
Euphausia Superba ◽  
Marine Species ◽  
Artificial Light ◽  
White Led ◽  
Light Emitting ◽  
Positive Phototaxis ◽  
Led Light ◽  
Exposure Experiment

AbstractThe use of light-emitting diodes (LEDs) is increasingly used in fishing gears and its application is known to trigger negative or positive phototaxis (i.e., swimming away or toward the light source, respectively) for some marine species. However, our understanding of how artificial light influences behavior is poorly understood for many species and most studies can be characterized as trial and error experiments. In this study, we tested whether exposure to white LED light could initiate a phototactic response in Antarctic krill (Euphausia superba). Trawl-caught krill were used in a controlled artificial light exposure experiment conducted onboard a vessel in the Southern Ocean. The experiment was conducted in chambers with dark and light zones in which krill could move freely. Results showed that krill displayed a significant positive phototaxis. Understanding this behavioral response is relevant to development of krill fishing technology to improve scientific sampling gear, improve harvest efficiency, and reduce potential unwanted bycatch.

scholarly journals Neurotoxic Effect of Ethanolic Extract of Propolis in the Presence of Copper Ions is Mediated through Enhanced Production of ROS and Stimulation of Caspase-3/7 Activity

Toxins ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 273 ◽  
Author(s):  
Vedrana Radovanović ◽  
Josipa Vlainić ◽  
Nikolina Hanžić ◽  
Petra Ukić ◽  
Nada Oršolić ◽  
...  
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Damage ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ethanolic Extract ◽  
Mitogen Activated Protein Kinase ◽  
Enhanced Production ◽  
Toxicological Studies ◽  
Ethanolic Extract Of Propolis

Elevated amounts of copper are considered to be contributing factor in the progression of neurodegenerative diseases as they promote oxidative stress conditions. The aim of our study was to examine the effects of ethanolic extract of propolis (EEP) against copper-induced neuronal damage. In cultured P19 neuronal cells, EEP exacerbated copper-provoked neuronal cell death by increasing the generation of reactive oxygen species (ROS) and through the activation of caspase-3/7 activity. EEP augmented copper-induced up-regulation of p53 and Bax mRNA expressions. Neurotoxic effects of EEP were accompanied by a strong induction of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression and decrease in the expression of c-fos mRNA. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK) prevented detrimental effects of EEP, whereas SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), exacerbated EEP-induced neuronal cell death. Quercetin, a polyphenolic nutraceutical, which is usually present in propolis, was also able to exacerbate copper-induced neuronal death. Our data indicates a pro-oxidative and apoptotic mode of EEP action in the presence of excess copper, wherein ROS/p53/p38 interactions play an important role in death cascades. Our study also pointed out that detailed pharmacological and toxicological studies must be carried out for propolis and other dietary supplements in order to fully recognize the potential adverse effects in specific conditions.

scholarly journals Cerebral Ischemia Causes Dysregulation of Synaptic Adhesion in Mouse Synaptosomes

2007 ◽  
Vol 28 (1) ◽  
pp. 99-110 ◽  
Author(s):  
Willard J Costain ◽  
Ingrid Rasquinha ◽  
Jagdeep K Sandhu ◽  
Peter Rippstein ◽  
Bogdan Zurakowski ◽  
...  
Keyword(s):  
Cell Death ◽  
Cerebral Ischemia ◽  
Adhesion Molecules ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Artery Occlusion ◽  
Synaptic Proteins ◽  
Mrna Levels ◽  
Neuronal Nuclei ◽  
Protein Levels

Synaptic pathology is observed during hypoxic events in the central nervous system in the form of altered dendrite structure and conductance changes. These alterations are rapidly reversible, on the return of normoxia, but are thought to initiate subsequent neuronal cell death. To characterize the effects of hypoxia on regulators of synaptic stability, we examined the temporal expression of cell adhesion molecules (CAMs) in synaptosomes after transient middle cerebral artery occlusion (MCAO) in mice. We focused on events preceding the onset of ischemic neuronal cell death (< 48 h). Synaptosome preparations were enriched in synaptically localized proteins and were free of endoplasmic reticulum and nuclear contamination. Electron microscopy showed that the synaptosome preparation was enriched in spheres (≈650 nm in diameter) containing secretory vesicles and postsynaptic densities. Forebrain mRNA levels of synaptically located CAMs was unaffected at 3 h after MCAO. This is contrasted by the observation of consistent downregulation of synaptic CAMs at 20 h after MCAO. Examination of synaptosomal CAM protein content indicated that certain adhesion molecules were decreased as early as 3 h after MCAO. For comparison, synaptosomal Agrn protein levels were unaffected by cerebral ischemia. Furthermore, a marked increase in the levels of p-Ctnnb1 in ischemic synaptosomes was observed. p-Ctnnb1 was detected in hippocampal fiber tracts and in cornu ammonis 1 neuronal nuclei. These results indicate that ischemia induces a dysregulation of a subset of synaptic proteins that are important regulators of synaptic plasticity before the onset of ischemic neuronal cell death.

scholarly journals Microglial TonEBP mediates LPS-induced inflammation and memory loss as transcriptional cofactor for NF-κB and AP-1

2020 ◽  
Vol 17 (1) ◽  
Author(s):  
Gyu Won Jeong ◽  
Hwan Hee Lee ◽  
Whaseon Lee-Kwon ◽  
Hyug Moo Kwon
Keyword(s):  
Microglial Activation ◽  
Neuronal Damage ◽  
Neuronal Cell Death ◽  
Myeloid Cells ◽  
Memory Loss ◽  
Neuronal Cell ◽  
Microglial Cell Line ◽  
Bv2 Cells ◽  
Pro Inflammatory Cytokines

Abstract Background Microglia are brain-resident myeloid cells involved in the innate immune response and a variety of neurodegenerative diseases. In macrophages, TonEBP is a transcriptional cofactor of NF-κB which stimulates the transcription of pro-inflammatory genes in response to LPS. Here, we examined the role of microglial TonEBP. Methods We used microglial cell line, BV2 cells. TonEBP was knocked down using lentiviral transduction of shRNA. In animals, TonEBP was deleted from myeloid cells using a line of mouse with floxed TonEBP. Cerulenin was used to block the NF-κB cofactor function of TonEBP. Results TonEBP deficiency blocked the LPS-induced expression of pro-inflammatory cytokines and enzymes in association with decreased activity of NF-κB in BV2 cells. We found that there was also a decreased activity of AP-1 and that TonEBP was a transcriptional cofactor of AP-1 as well as NF-κB. Interestingly, we found that myeloid-specific TonEBP deletion blocked the LPS-induced microglia activation and subsequent neuronal cell death and memory loss. Cerulenin disrupted the assembly of the TonEBP/NF-κB/AP-1/p300 complex and suppressed the LPS-induced microglial activation and the neuronal damages in animals. Conclusions TonEBP is a key mediator of microglial activation and neuroinflammation relevant to neuronal damage. Cerulenin is an effective blocker of the TonEBP actions.

Role of caspase-3 in neuronal cell death

1998 ◽  
Vol 5 ◽  
pp. 207
Author(s):  
A. Gorman ◽  
E. Bonfoco ◽  
B. Zhivotovsky ◽  
S. Orrenius ◽  
S. Ceccatelli
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Caspase-3-Like Protease Activity-Independent Apoptosis at the Onset of Neuronal Cell Death in the Gerbil Hippocampus after Global Ischemia

2007 ◽  
Vol 30 (10) ◽  
pp. 1950-1953 ◽  
Author(s):  
Hiroki Shimizu ◽  
Makoto Ohgoh ◽  
Masuhiro Ikeda ◽  
Yukio Nishizawa ◽  
Hiroo Ogura
Keyword(s):  
Cell Death ◽  
Protease Activity ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia
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