scholarly journals Proteomic responses to ocean acidification in the brain of juvenile coral reef fish

2020 ◽  
Author(s):  
Hin Hung Tsang ◽  
Megan Welch ◽  
Philip L. Munday ◽  
Timothy Ravasi ◽  
Celia Schunter
Keyword(s):  
Juvenile Fish ◽  
Differentially Expressed ◽  
Juvenile Coral ◽  
Genome Wide ◽  
Chemical Alarm Cues ◽  
Contrast Exposure ◽  
Parental Phenotype ◽  
Proteomic Responses ◽  
The Brain

AbstractElevated CO2 levels predicted to occur by the end of the century can affect the physiology and behaviour of marine fishes. For one important survival mechanism, the response to chemical alarm cues from conspecifics, substantial among-individual variation in the extent of behavioural impairment when exposed to elevated CO2 has been observed in previous studies. Whole brain transcriptomic data has further emphasized the importance of parental phenotypic variation in the response of juvenile fish to elevated CO2. In this study, we investigate the genome-wide proteomic responses of this variation in the brain of 5-week old spiny damselfish, Acanthochromis polyacanthus. We compared the expression of proteins in the brains of juvenile A. polyacanthus from two different parental behavioural phenotypes (sensitive and tolerant) that had been experimentally exposed to short-term, long-term and inter-generational elevated CO2. Our results show differential expression of key proteins related to stress response and epigenetic markers with elevated CO2 exposure. Proteins related to neurological development were also differentially expressed particularly in the long-term developmental treatment, which might be critical for juvenile development. By contrast, exposure to elevated CO2 in the parental generation resulted in only three differentially expressed proteins in the offspring, revealing potential for inter-generational acclimation. Lastly, we found a distinct proteomic pattern in juveniles due to the behavioural sensitivity of parents to elevated CO2, even though the behaviour of the juvenile fish was impaired regardless of parental phenotype. Our data shows that developing juveniles are affected in their brain protein expression by elevated CO2, but the effect varies with the length of exposure as well as due to variation of parental phenotypes in the population.

scholarly journals Nickel-induced transcriptional changes persist  post exposure through epigenetic reprogramming

2019 ◽  
Vol 12 (1) ◽  
Author(s):  
Cynthia C. Jose ◽  
Zhenjia Wang ◽  
Vinay Singh Tanwar ◽  
Xiaoru Zhang ◽  
Chongzhi Zang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Histone Modification ◽  
Lung Epithelial Cells ◽  
Differentially Expressed ◽  
Nickel Ions ◽  
Post Exposure ◽  
Genome Wide ◽  
Transcriptional Changes ◽  
Nickel Exposure

Abstract Background Nickel is an occupational and environmental toxicant associated with a number of diseases in humans including pulmonary fibrosis, bronchitis and lung and nasal cancers. Our earlier studies showed that the nickel-exposure-induced genome-wide transcriptional changes, which persist even after the termination of exposure may underlie nickel pathogenesis. However, the mechanisms that drive nickel-induced persistent changes to the transcriptome remain elusive. Results To elucidate the mechanisms that underlie nickel-induced long-term transcriptional changes, in this study, we examined the transcriptome and the epigenome of human lung epithelial cells during nickel exposure and after the termination of exposure. We identified two categories of persistently differentially expressed genes: (i) the genes that were differentially expressed during nickel exposure; and (ii) the genes that were differentially expressed only after the termination of exposure. Interestingly, > 85% of the nickel-induced gene expression changes occurred only after the termination of exposure. We also found extensive genome-wide alterations to the activating histone modification, H3K4me3, after the termination of nickel exposure, which coincided with the post-exposure gene expression changes. In addition, we found significant post-exposure alterations to the repressive histone modification, H3K27me3. Conclusion Our results suggest that while modest first wave of transcriptional changes occurred during nickel exposure, extensive transcriptional changes occurred during a second wave of transcription for which removal of nickel ions was essential. By uncovering a new category of transcriptional and epigenetic changes, which occur only after the termination of exposure, this study provides a novel understanding of the long-term deleterious consequences of nickel exposure on human health.

scholarly journals Proteomics Analysis Reveals the Implications of Cytoskeleton and Mitochondria in the Response of the Rat Brain to Starvation

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 219 ◽  
Author(s):  
Beatriz Cuevas-Fernández ◽  
Carlos Fuentes-Almagro ◽  
Juan Peragón
Keyword(s):  
Mass Spectrometry ◽  
Rat Brain ◽  
Food Deprivation ◽  
Metabolic Response ◽  
Differentially Expressed ◽  
Nervous Impulse ◽  
Altered Expression ◽  
Peptide Mass ◽  
The Brain

Long-term starvation provokes a metabolic response in the brain to adapt to the lack of nutrient intake and to maintain the physiology of this organ. Here, we study the changes in the global proteomic profile of the rat brain after a seven-day period of food deprivation, to further our understanding of the biochemical and cellular mechanisms underlying the situations without food. We have used two-dimensional electrophoresis followed by mass spectrometry (2D-MS) in order to identify proteins differentially expressed during prolonged food deprivation. After the comparison of the protein profiles, 22 brain proteins were found with altered expression. Analysis by peptide mass fingerprinting and MS/MS (matrix-assisted laser desorption-ionization-time of flight mass spectrometer, MALDI-TOF/TOF) enabled the identification of 14 proteins differentially expressed that were divided into 3 categories: (1) energy catabolism and mitochondrial proteins; (2) chaperone proteins; and (3) cytoskeleton, exocytosis, and calcium. Changes in the expression of six proteins, identified by the 2D-MS proteomics procedure, were corroborated by a nanoliquid chromatography-mass spectrometry proteomics procedure (nLC-MS). Our results show that long-term starvation compromises essential functions of the brain related with energetic metabolism, synapsis, and the transmission of nervous impulse.

scholarly journals Emiliania huxleyi increases calcification but not expression of calcification-related genes in long-term exposure to elevated temperature and p CO 2

2013 ◽  
Vol 368 (1627) ◽  
pp. 20130049 ◽  
Author(s):  
Ina Benner ◽  
Rachel E. Diner ◽  
Stephane C. Lefebvre ◽  
Dian Li ◽  
Tomoko Komada ◽  
...  
Keyword(s):  
Carbon Content ◽  
Emiliania Huxleyi ◽  
Differentially Expressed ◽  
Organic Carbon Content ◽  
Rna Seq ◽  
Ambient Conditions ◽  
Negative Effects ◽  
Genome Wide ◽  
Global Carbon

Increased atmospheric p CO 2 is expected to render future oceans warmer and more acidic than they are at present. Calcifying organisms such as coccolithophores that fix and export carbon into the deep sea provide feedbacks to increasing atmospheric p CO 2 . Acclimation experiments suggest negative effects of warming and acidification on coccolithophore calcification, but the ability of these organisms to adapt to future environmental conditions is not well understood. Here, we tested the combined effect of p CO 2 and temperature on the coccolithophore Emiliania huxleyi over more than 700 generations. Cells increased inorganic carbon content and calcification rate under warm and acidified conditions compared with ambient conditions, whereas organic carbon content and primary production did not show any change. In contrast to findings from short-term experiments, our results suggest that long-term acclimation or adaptation could change, or even reverse, negative calcification responses in E. huxleyi and its feedback to the global carbon cycle. Genome-wide profiles of gene expression using RNA-seq revealed that genes thought to be essential for calcification are not those that are most strongly differentially expressed under long-term exposure to future ocean conditions. Rather, differentially expressed genes observed here represent new targets to study responses to ocean acidification and warming.

scholarly journals Proteomic Responses to Ocean Acidification in the Brain of Juvenile Coral Reef Fish

2020 ◽  
Vol 7 ◽  
Author(s):  
Hin Hung Tsang ◽  
Megan J. Welch ◽  
Philip L. Munday ◽  
Timothy Ravasi ◽  
Celia Schunter
Keyword(s):  
Coral Reef ◽  
Ocean Acidification ◽  
Reef Fish ◽  
Coral Reef Fish ◽  
Juvenile Coral ◽  
Proteomic Responses ◽  
The Brain

scholarly journals Nickel induced transcriptional changes persist post exposure through epigenetic reprograming

2019 ◽  
Author(s):  
Cynthia C Jose ◽  
Zhenjia Wang ◽  
Vinay Singh Tanwar ◽  
Xiaoru Zhang ◽  
Chongzhi Zang ◽  
...  
Keyword(s):  
Histone Modification ◽  
Lung Epithelial Cells ◽  
Differentially Expressed ◽  
Post Exposure ◽  
Genome Wide ◽  
Lung Epithelial ◽  
Repressive Histone Modification ◽  
Transcriptional Changes ◽  
Nickel Exposure

AbstractNickel is an occupational and environmental toxicant associated with a number of diseases in humans including pulmonary fibrosis, bronchitis and lung and nasal cancers. Our earlier studies showed that the nickel-exposure-induced genome-wide transcriptional changes, which persist even after the termination of exposure may underlie nickel pathogenesis. However, the mechanisms that drive nickel-induced persistent changes to the transcriptome remain elusive. To elucidate the mechanisms that underlie nickel induced long-term transcriptional changes, in this study, we examined the transcriptome and the epigenome of human lung epithelial cells during nickel exposure and after the termination of exposure. We identified two categories of persistently differentially expressed genes based on the timing of expression changes: i) the genes that were differentially expressed during nickel exposure; and ii) the genes that were differentially expressed only after the termination of nickel exposure. Interestingly, the majority of nickel-induced transcriptional changes occurred only after the termination of exposure. We found robust genome-wide alterations to the activating histone modification, H3K4me3, after the termination of nickel exposure, which coincided with the post-exposure gene expression changes. In addition, we found significant post-exposure alterations to the repressive histone modification, H3K27me3. By uncovering a new category of transcriptional and epigenetic changes, which occur only after the termination of exposure, this study sheds new light on the post-exposure effects of nickel and provides a novel understanding of the long-term deleterious consequences of nickel exposure on human health.

scholarly journals Global miRNA/proteomic analyses identify miRNAs at 14q32 and 3p21, which contribute to features of chronic iron-exposed fallopian tube epithelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ravneet Chhabra ◽  
Stephanie Rockfield ◽  
Jennifer Guergues ◽  
Owen W. Nadeau ◽  
Robert Hill ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Fallopian Tube ◽  
Histone Deacetylation ◽  
Differentially Expressed ◽  
Epigenetic Alterations ◽  
Genome Wide ◽  
Proteomics Approach ◽  
Differentially Expressed Mirnas ◽  
Protein Alterations

AbstractMalignant transformation of fallopian tube secretory epithelial cells (FTSECs) is a key contributing event to the development of high-grade serous ovarian carcinoma (HGSOC). Our recent findings implicate oncogenic transformative events in chronic iron-exposed FTSECs, including increased expression of oncogenic mediators, increased telomerase transcripts, and increased growth/migratory potential. Herein, we extend these studies by implementing an integrated transcriptomic and mass spectrometry-based proteomics approach to identify global miRNA and protein alterations, for which we also investigate a subset of these targets to iron-induced functional alterations. Proteomic analysis identified > 4500 proteins, of which 243 targets were differentially expressed. Sixty-five differentially expressed miRNAs were identified, of which 35 were associated with the “top” proteomic molecules (> fourfold change) identified by Ingenuity Pathway Analysis. Twenty of these 35 miRNAs are at the 14q32 locus (encoding a cluster of 54 miRNAs) with potential to be regulated by DNA methylation and histone deacetylation. At 14q32, miR-432-5p and miR-127-3p were ~ 100-fold downregulated whereas miR-138-5p was 16-fold downregulated at 3p21 in chronic iron-exposed FTSECs. Combinatorial treatment with methyltransferase and deacetylation inhibitors reversed expression of these miRNAs, suggesting chronic iron exposure alters miRNA expression via epigenetic alterations. In addition, PAX8, an important target in HGSOC and a potential miRNA target (from IPA) was epigenetically deregulated in iron-exposed FTSECs. However, both PAX8 and ALDH1A2 (another IPA-predicted target) were experimentally identified to be independently regulated by these miRNAs although TERT RNA was partially regulated by miR-138-5p. Interestingly, overexpression of miR-432-5p diminished cell numbers induced by long-term iron exposure in FTSECs. Collectively, our global profiling approaches uncovered patterns of miRNA and proteomic alterations that may be regulated by genome-wide epigenetic alterations and contribute to functional alterations induced by chronic iron exposure in FTSECs. This study may provide a platform to identify future biomarkers for early ovarian cancer detection and new targets for therapy.

scholarly journals LONG-TERM CHRONIC CALORIC RESTRICTION ALTERS miRNA PROFILES IN THE BRAIN OF AGEING MICE

2021 ◽  
pp. 1-32
Author(s):  
Umit Ozorhan ◽  
Bilge G. Tuna ◽  
Munevver B. Cicekdal ◽  
Aysegul Kuskucu ◽  
Omer F. Bayrak ◽  
...  
Keyword(s):  
Differentially Expressed ◽  
Protective Effects ◽  
Expression Levels ◽  
Age Related ◽  
Altered Gene ◽  
Old Mice ◽  
Ageing Brain ◽  
The Brain ◽  
Preventive Effects

ABSTRACT Calorie restriction (CR) has been shown to be one of the most effective methods in alleviating the effects of ageing and age-related diseases such as increasing longevity and preventing dementia, and Alzheimer’s Disease. Although the protective effects of CR have been reported, the exact molecular mechanism still needs to be clarified. This study aims to determine differentially expressed (DE) miRNAs and altered gene pathways due to long-term chronic (CCR) and intermittent (ICR) CR in the brain of mice to understand the preventive roles of miRNAs in long-term CR. Ten weeks old mice were enrolled into three different dietary groups; ad-libitum, CCR or ICR, and fed until 82 weeks old mice. miRNAs were analyzed using GeneChip 4.1 microarray and the target of DE miRNAs was determined using miRNA target databases. Out of a total 3,163 analyzed miRNAs, 55 of them were differentially expressed either by different CR protocols or by ageing. Brain samples from the CCR group had increased expression levels of mmu-miR-713 while decreasing expression levels of mmu-miR-184-3p and mmu-miR-351-5p compared to the other dietary groups. Also, current results indicated that CCR showed better preventive effects than that of ICR. Thus, CCR may perform its protective effects by modulating these specific miRNAs since they are shown to play roles in neurogenesis, chromatin, and histone regulation. In conclusion, these three miRNAs could be potential targets for neurodegenerative and ageing-related diseases and may play important roles in the protective effects of CR in the brain.

The Acute Effect of Alcohol on Various Memory Processes

2010 ◽  
Vol 24 (4) ◽  
pp. 249-252 ◽  
Author(s):  
Márk Molnár ◽  
Roland Boha ◽  
Balázs Czigler ◽  
Zsófia Anna Gaál
Keyword(s):  
Low Dose ◽  
Short Term Memory ◽  
Acute Effect ◽  
Long Term Memory ◽  
Term Memory ◽  
Memory Processes ◽  
Different Types ◽  
The Brain ◽  
Legal Consequences

This review surveys relevant and recent data of the pertinent literature regarding the acute effect of alcohol on various kinds of memory processes with special emphasis on working memory. The characteristics of different types of long-term memory (LTM) and short-term memory (STM) processes are summarized with an attempt to relate these to various structures in the brain. LTM is typically impaired by chronic alcohol intake but according to some data a single dose of ethanol may have long lasting effects if administered at a critically important age. The most commonly seen deleterious acute effect of alcohol to STM appears following large doses of ethanol in conditions of “binge drinking” causing the “blackout” phenomenon. However, with the application of various techniques and well-structured behavioral paradigms it is possible to detect, albeit occasionally, subtle changes of cognitive processes even as a result of a low dose of alcohol. These data may be important for the consideration of legal consequences of low-dose ethanol intake in conditions such as driving, etc.

Moving past the vaccine/autism controversy - to examine potential vaccine neurological harms

2020 ◽  
pp. 1-15
Author(s):  
Peter R. Breggin
Keyword(s):  
Neurological Disorders ◽  
Developmental Disorder ◽  
Physical Symptoms ◽  
Psychosocial Disorders ◽  
The Us ◽  
Potential Vaccine ◽  
Research And Education ◽  
The Brain ◽  
New Vaccines

BACKGROUND: The vaccine/autism controversy has caused vast scientific and public confusion, and it has set back research and education into genuine vaccine-induced neurological disorders. The great strawman of autism has been so emphasized by the vaccine industry that it, and it alone, often appears in authoritative discussions of adverse effects of the MMR and other vaccines. By dismissing the chimerical vaccine/autism controversy, vaccine defenders often dismiss all genuinely neurological aftereffects of the MMR (measles, mumps, and rubella) and other vaccines, including well-documented events, such as relatively rare cases of encephalopathy and encephalitis. OBJECTIVE: This report explains that autism is not a physical or neurological disorder. It is not caused by injury or disease of the brain. It is a developmental disorder that has no physical origins and no physical symptoms. It is extremely unlikely that vaccines are causing autism; but it is extremely likely that they are causing more neurological damage than currently appreciated, some of it resulting in psychosocial disabilities that can be confused with autism and other psychosocial disorders. This confusion between a developmental, psychosocial disorder and a physical neurological disease has played into the hands of interest groups who want to deny that vaccines have any neurological and associated neuropsychiatric effects. METHODS: A review of the scientific literature, textbooks, and related media commentary is integrated with basic clinical knowledge. RESULTS: This report shows how scientific sources have used the vaccine/autism controversy to avoid dealing with genuine neurological risks associated with vaccines and summarizes evidence that vaccines, including the MMR, can cause serious neurological disorders. Manufacturers have been allowed by the US Food and Drug Administration (FDA) to gain vaccine approval without placebo-controlled clinical trials. CONCLUSIONS: The misleading vaccine autism controversy must be set aside in favor of examining actual neurological harms associated with vaccines, including building on existing research that has been ignored. Manufacturers of vaccines must be required to conduct placebo-controlled clinical studies for existing vaccines and for government approval of new vaccines. Many probable or confirmed neurological adverse events occur within a few days or weeks after immunization and could be detected if the trials were sufficiently large. Contrary to current opinion, large, long-term placebo-controlled trials of existing and new vaccines would be relatively easy and safe to conduct.

Long-term management of patients with multiple brain metastases after shaped beam radiosurgery

2004 ◽  
pp. 406-412
Author(s):  
Paul Okunieff ◽  
Michael C. Schell ◽  
Russell Ruo ◽  
E. Ronald Hale ◽  
Walter G. O'Dell ◽  
...  
Keyword(s):  
Brain Metastases ◽  
Tumor Control ◽  
Content Type ◽  
Negative Results ◽  
Multiple Metastases ◽  
Extracranial Disease ◽  
Successful Control ◽  
The Brain

✓ The role of radiosurgery in the treatment of patients with advanced-stage metastatic disease is currently under debate. Previous randomized studies have not consistently supported the use of radiosurgery to treat patients with numbers of brain metastases. In negative-results studies, however, intracranial tumor control was high but extracranial disease progressed; thus, patient survival was not greatly affected, although neurocognitive function was generally maintained until death. Because the future promises improved systemic (extracranial) therapy, the successful control of brain disease is that much more crucial. Thus, for selected patients with multiple metastases to the brain who remain in good neurological condition, aggressive lesion-targeting radiosurgery should be very useful. Although a major limitation to success of this therapy is the lack of control of extracranial disease in most patients, it is clear that well-designed, aggressive treatment substantially decreases the progression of brain metastases and also improves neurocognitive survival. The authors present the management and a methodology for rational treatment of a patient with breast cancer who has harbored 24 brain metastases during a 3-year period.

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