scholarly journals Proteomic Response of the Brain to Hypoxic Stress in Marine Medaka Fish (Oryzias melastigma)

2021 ◽  
Vol 8 ◽  
Author(s):  
Keng Po Lai ◽  
Nathan Tam ◽  
Simon Yuan Wang ◽  
William Ka Fai Tse ◽  
Xiao Lin ◽  
...  

Hypoxia is a serious issue that affects the marine environment, with a growing number of hypoxic “dead zones” occurring each year. Reports have indicated that hypoxia is detrimental to the reproductive function and sexual development of fish via the disruption of endocrine signaling in organs involved in the hypothalamus–pituitary–gonad axis, including the brain. While we previously reported that hypoxia induces transcriptome-wide alterations in the brain of marine medaka (Oryzias melastigma), whether these effects were reflected at the protein level remains unclear. Therefore, the present study used high-throughput proteomic sequencing along with bioinformatics analysis to assess the short-term and multi-generational effects of hypoxia on the brain proteome of O. melastigma. We identified 36,567 peptides and 7,599 proteins (1% false discovery rate in brain samples), with functions involved in cellular and metabolic processes such as signaling and reproductive processes as well as energy production and conversion. Furthermore, we determined that hypoxia resulted in the significant differential expressions of 33 upregulated and 69 downregulated proteins in the short-term exposure group and 24 upregulated and 52 downregulated proteins in the multi-generational exposure group. Pathway enrichment analysis of the deregulated proteins indicated that hypoxia could impair brain function by altering arachidonic acid metabolism, tight junctions, and adrenergic signaling under short-term hypoxic exposure and by altering p53 and PI3K–Akt signaling under multi-generational hypoxic exposure, which may lead to the onset of neurodegenerative disorders including Alzheimer’s disease and amyotrophic lateral sclerosis. Ingenuity pathway analysis of the deregulated proteins showed that hypoxia affected common signaling pathways in the brain (e.g., integrin, paxillin, and epithelial adherens junction signaling) under both short-term and multi-generational exposures. Hypoxia also deregulated pathways specific to short-term exposure (including integrin-linked kinase, calcium, and integrin signaling) and multi-generational exposure (including sphingosine-1-phosphate signaling, endocannabinoid neuronal synapse pathway, and endoplasmic reticulum stress pathway). Overall, our results provide additional insights into the mechanisms of hypoxia disrupting neuronal function at the protein level in marine medaka.

2017 ◽  
Vol 13 (3) ◽  
pp. 340-344
Author(s):  
Bijay Aryal

Background & Objectives:Radiofrequency radiation affects the calcium permeability and accordingly this induces pathophysiological changes in the brain and its subsequent output in the brain as tumor genesis, neural degeneration, and cognition or behavior changes. Hence, we investigated the effects of radiofrequency (RF) radiation on calcium binding proteins, reactive gliosis, and tumor genesis in mouse brain. Materials & Methods:Mice were exposed to radiofrequency radiation in the cage chamber with average specific absorption rate (SAR) of 1.6 W/kg and 4.0 W/Kg for one hour per day for five days. For histochemical studies, radiofrequency exposed brains were compared with sham control using calbindin D-28k antibody.Results:The immunoreactivity of calbindin D-28k, a marker for calcium homeostasis was found to increase in dose-response manner in hippocampus and cerebellar cortex.Conclusion:The short-term exposure to 835 MHz RF could induce disruption of calcium homeostasis and resulting neurobehavioral changes or brain tumor. 


PLoS ONE ◽  
2014 ◽  
Vol 9 (10) ◽  
pp. e110698 ◽  
Author(s):  
Karen Lau ◽  
Keng Po Lai ◽  
Jessie Yun Juan Bao ◽  
Na Zhang ◽  
Anna Tse ◽  
...  

2021 ◽  
Vol 12 (1) ◽  
pp. 52
Author(s):  
Bora Mun ◽  
Yun-Chol Jang ◽  
Eun-Jong Kim ◽  
Ja-Hae Kim ◽  
Min-Keun Song

Hypoxic brain injury is accompanied by a decrease in various functions. It is also known that obstructive sleep apnea (OSA) can cause hypoxic brain injury. This study aimed to produce a model of an intermittent hypoxic brain condition in rats and determine the activity of the brain according to the duration of hypoxic exposure. Forty male Sprague–Dawley rats were divided into four groups: the control group (n = 10), the 2 h per day hypoxia exposure group (n = 10), the 4 h per day hypoxia exposure group (n = 10), and the 8 h per day hypoxia exposure group (n = 10). All rats were exposed to a hypoxic chamber containing 10% oxygen for five days. Positron emission tomography–computed tomography (PET-CT) brain images were acquired using a preclinical PET-CT scanner to evaluate the activity of brain metabolism. All the rats were subjected to normal conditions. After five days, PET-CT was performed to evaluate the recovery of brain metabolism. Western blot analysis and immunohistochemistry were performed with vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). The mean SUV was elevated in the 2 h per day and 4 h per day groups, and all brain regions showed increased metabolism except the amygdala on the left side, the auditory cortex on the right side, the frontal association cortex on the right side, the parietal association cortex on the right side, and the somatosensory cortex on the right side immediately after hypoxic exposure. However, there was no difference between 5 days rest after hypoxic exposure and control group. Western blot analysis revealed the most significant immunoreactivity for VEGF in the 2, 4, and 8 h per day groups compared with the control group and quantification of VEGF immunohistochemistry showed more expression in 2 and 4 h per day groups compared with the control group. However, there was no significant difference in immunoreactivity for BDNF among the groups. The duration of exposure to hypoxia may affect the activity of the brain due to angiogenesis after intermittent hypoxic brain conditions in rats.


2009 ◽  
Vol 81 (Suppl_1) ◽  
pp. 263-263
Author(s):  
Edward F. Orlando ◽  
Jane Thompson ◽  
Marisol Sepulveda ◽  
Gary Ankley ◽  
Daniel Villeneuve ◽  
...  

2018 ◽  
Vol 115 (10) ◽  
pp. E2393-E2402 ◽  
Author(s):  
Michael L. Risner ◽  
Silvia Pasini ◽  
Melissa L. Cooper ◽  
Wendi S. Lambert ◽  
David J. Calkins

Diseases of the brain involve early axon dysfunction that often precedes outright degeneration. Pruning of dendrites and their synapses represents a potential driver of axonopathy by reducing activity. Optic nerve degeneration in glaucoma, the world’s leading cause of irreversible blindness, involves early stress to retinal ganglion cell (RGC) axons from sensitivity to intraocular pressure (IOP). This sensitivity also influences survival of RGC dendrites and excitatory synapses in the retina. Here we tested in individual RGCs identified by type the relationship between dendritic organization and axon signaling to light following modest, short-term elevations in pressure. We found dendritic pruning occurred early, by 2 wk of elevation, and independent of whether the RGC responded to light onset (ON cells) or offset (OFF cells). Pruning was similarly independent of ON and OFF in the DBA/2J mouse, a chronic glaucoma model. Paradoxically, all RGCs, even those with significant pruning, demonstrated a transient increase in axon firing in response to the preferred light stimulus that occurred on a backdrop of generally enhanced excitability. The increased response was not through conventional presynaptic signaling, but rather depended on voltage-sensitive sodium channels that increased transiently in the axon. Pruning, axon dysfunction, and deficits in visual acuity did not progress between 2 and 4 wk of elevation. These results suggest neurodegeneration in glaucoma involves an early axogenic response that counters IOP-related stress to excitatory dendritic architecture to slow progression and maintain signaling to the brain. Thus, short-term exposure to elevated IOP may precondition the neural system to further insult.


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