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Venizelos, Nikolaos, ProfessorORCID iD iconorcid.org/0000-0001-8102-1804
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Publikasjoner (10 av 38) Visa alla publikasjoner
Logotheti, M., Chatziioannou, A., Venizelos, N. & Kolisis, F. (2019). Recent Advancements in Bipolar Disorder studies through Genomic, Epigenomic and Metagenomic Approaches. Journal of Psychiatry and Psychology Research, 2(1), 56-66
Åpne denne publikasjonen i ny fane eller vindu >>Recent Advancements in Bipolar Disorder studies through Genomic, Epigenomic and Metagenomic Approaches
2019 (engelsk)Inngår i: Journal of Psychiatry and Psychology Research, ISSN 2640-6136, Vol. 2, nr 1, s. 56-66Artikkel, forskningsoversikt (Fagfellevurdert) Published
Abstract [en]

Bipolar disorder is a complex and highly heritable psychiatric disorder characterized by severe mood alterations. The precise geneticunderpinnings of the disease have not been identified so far, despite numerous genome-wide association findings. This review describes thecurrent state of genetic studies based on next generation sequencing technologies including whole exome and whole genome sequencing, aswell as RNA-sequencing and highlights the fact that the integration of these studies can reveal novel knowledge such as the functional roleof gene variants. However, due to the complexity of bipolar disorder, it is a compelling candidate for studies beyond DNA and RNAsequencing. Epigenetic alterations, defined as heritable but reversible modifications including DNA methylation, DNAhydroxymethylation, histone modifications and non-coding RNAs may be the link between genome and environment interactions.Additionally, a possible source of the reported immune activation in bipolar disorder is the micro biome of gastrointestinal tract, due torecent studies that indicate its pivotal role in brain function through the ‘gut-brain’ axis. The identification of methods able to modulate themicro biome emerges as a promising path for novel diagnostic and treatment options in bipolar disorder, thus the number of metagenomicstudies in bipolar disorder has substantially increased the last years. Overall, the paper aims to review the most recent literature ongenomic, epigenomic and metagenomic studies that have contributed to our understanding of the pathophysiology of bipolar disorder sofar. The paper also focuses on the exploitation of recent advancements in high-throughput technologies for the elucidation of bipolardisorder through different approaches that may provide complementary knowledge and concludes to the need for merging the gap betweenall the gathered knowledge from the analysis of high-throughput data.

sted, utgiver, år, opplag, sider
SciTech Central Inc., 2019
Emneord
Bipolar disorder, Whole exome sequencing, Whole genome sequencing, Metagenomics, Epigenomics, RNA sequencing
HSV kategori
Forskningsprogram
Psykiatri; Medicin; Biomedicin
Identifikatorer
urn:nbn:se:oru:diva-73695 (URN)
Prosjekter
Experimentell neuropsykiatri
Tilgjengelig fra: 2019-04-13 Laget: 2019-04-13 Sist oppdatert: 2019-04-24bibliografisk kontrollert
Pernow, Y., Shahror, R., Acharya, S., Jahnson, L., Vumma, R. & Venizelos, N. (2018). Aberrant tryptophan transport in cultured fibroblast from patients with Male Idiopathic Osteoporosis: An in vitro study. Bone Reports, 8, 25-28
Åpne denne publikasjonen i ny fane eller vindu >>Aberrant tryptophan transport in cultured fibroblast from patients with Male Idiopathic Osteoporosis: An in vitro study
Vise andre…
2018 (engelsk)Inngår i: Bone Reports, ISSN 2352-1872, Vol. 8, s. 25-28Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

It has been demonstrated, that long-term chronic tryptophan deficiency, results in decreased serotonin synthesis, which may lead to low bone mass and low bone formation. Findings from studies in male patients with idiopathic osteoporosis suggested a decreased transport of tryptophan in erythrocytes of osteoporotic patients, indicating that serotonin system defects may be involved in the etiology of low bone mass. Tryptophan is the precursor of serotonin, and a disturbed transport of tryptophan is implicated in altered serotonin synthesis. However, no study has investigated the tryptophan transport kinetics in MIO patients. The aim of this study is to investigate the kinetic parameters of tryptophan transport in fibroblasts derived from MIO patients compared to age and sex matched controls. Fibroblast cells were cultured from skin biopsies obtained from 14 patients diagnosed with Male Idiopathic Osteoporosis and from 13 healthy age-sex matched controls, without a diagnosis of osteoporosis. Transport of the amino acid tryptophan across the cell membrane was measured by the cluster tray method. The kinetic parameters, maximal transport capacity (Vmax) and affinity constant (Km) were determined by using the Lineweaver-Burke plot equation. The results of this study have shown a significantly lower mean value for Vmax (p = 0.0138) and lower Km mean value (p = 0.0009) of tryptophan transport in fibroblasts of MIO patients compared to the control group. A lower Vmax implied a decreased tryptophan transport availability in MIO patients. In conclusion, reduced cellular tryptophan availability in MIO patients might result in reduced brain serotonin synthesis and its endogenous levels in peripheral tissues, and this may contribute to low bone mass/formation. The findings of the present study could contribute to the etiology of idiopathic osteoporosis and for the development of novel approaches for diagnosis, treatment and management strategies of MIO.

sted, utgiver, år, opplag, sider
Amsterdam, Netherlands: Elsevier, 2018
Emneord
Amino acid transport, Fibroblasts, Male Idiopathic Osteoporosis, Serotonin, Tryptophan
HSV kategori
Identifikatorer
urn:nbn:se:oru:diva-65009 (URN)10.1016/j.bonr.2018.01.002 (DOI)29379847 (PubMedID)2-s2.0-85042358304 (Scopus ID)
Tilgjengelig fra: 2018-02-14 Laget: 2018-02-14 Sist oppdatert: 2018-08-20bibliografisk kontrollert
Comasco, E., Vumma, R., Toffoletto, R., Johansson, J., Flyckt, L., Lewander, T., . . . Venizelos, N. (2017). Genetic and Functional Study of L-Type Amino Acid Transporter 1 in Schizophrenia. Neuropsychobiology, 74(2), 96-103
Åpne denne publikasjonen i ny fane eller vindu >>Genetic and Functional Study of L-Type Amino Acid Transporter 1 in Schizophrenia
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2017 (engelsk)Inngår i: Neuropsychobiology, ISSN 0302-282X, E-ISSN 1423-0224, Vol. 74, nr 2, s. 96-103Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Schizophrenia involves neural catecholaminergic dysregulation. Tyrosine is the precursor of catecholamines, and its major transporter, according to studies on fibroblasts, in the brain is the L-type amino acid transporter 1 (LAT1). The present study assessed haplotype tag single-nucleotide polymorphisms (SNPs) of the SLC7A5/LAT1 gene in 315 patients with psychosis within the schizophrenia spectrum and 233 healthy controls to investigate genetic vulnerability to the disorder as well as genetic relationships to homovanillic acid (HVA) and 3-methoxy-4-hydroxyphenylglycol (MHPG), the major catecholamine metabolites in the cerebrospinal fluid (CSF). Moreover, the involvement of the different isoforms of the system L in tyrosine uptake and LAT1 tyrosine kinetics were studied in fibroblast cell lines of 10 patients with schizophrenia and 10 healthy controls. The results provide suggestive evidence of individual vulnerability to schizophrenia related to the LAT1 SNP rs9936204 genotype. A number of SNPs were nominally associated with CSF HVA and MHPG concentrations but did not survive correction for multiple testing. The LAT1 isoform was confirmed as the major tyrosine transporter in patients with schizophrenia. However, the kinetic parameters (maximal transport capacity, affinity of the binding sites, and diffusion constant of tyrosine transport through the LAT1 isoform) did not differ between patients with schizophrenia and controls. The present genetic findings call for independent replication in larger samples, while the functional study seems to exclude a role of LAT1 in the aberrant transport of tyrosine in fibroblasts of patients with schizophrenia.

sted, utgiver, år, opplag, sider
Basel: S. Karger, 2017
Emneord
Amino acid transporter light chain system L; Fibroblasts; L-Type amino acid transporter 1; Schizophrenia; Single-nucleotide polymorphism; Tyrosine
HSV kategori
Forskningsprogram
Psykiatri; Genetik; Biomedicin
Identifikatorer
urn:nbn:se:oru:diva-55674 (URN)10.1159/000455234 (DOI)000399488600008 ()28190014 (PubMedID)2-s2.0-85013072462 (Scopus ID)
Tilgjengelig fra: 2017-02-14 Laget: 2017-02-14 Sist oppdatert: 2018-07-30bibliografisk kontrollert
Tobe, B. T. D., Venizelos, N. & Snyder, E. Y. (2017). Probing the lithium-response pathway in hiPSCs implicates the phosphoregulatory set-point for a cytoskeletal modulator in bipolar pathogenesis. Proceedings of the National Academy of Sciences of the United States of America, 114(22), E4462-E4471, Article ID 1700111114.
Åpne denne publikasjonen i ny fane eller vindu >>Probing the lithium-response pathway in hiPSCs implicates the phosphoregulatory set-point for a cytoskeletal modulator in bipolar pathogenesis
2017 (engelsk)Inngår i: Proceedings of the National Academy of Sciences of the United States of America, ISSN 0027-8424, E-ISSN 1091-6490, Vol. 114, nr 22, s. E4462-E4471, artikkel-id 1700111114Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The molecular pathogenesis of bipolar disorder (BPD) is poorly understood. Using human-induced pluripotent stem cells (hiPSCs) to unravel such mechanisms in polygenic diseases is generally challenging. However, hiPSCs from BPD patients responsive to lithium offered unique opportunities to discern lithium's target and hence gain molecular insight into BPD. By profiling the proteomics of BDP-hiPSC-derived neurons, we found that lithium alters the phosphorylation state of collapsin response mediator protein-2 (CRMP2). Active non-phosphorylated CRMP2, which binds cytoskeleton, is present throughout the neuron; inactive phosphorylated CRMP2, which dissociates from cytoskeleton, exits dendritic spines. CRMP2 elimination yields aberrant dendritogenesis with diminished spine density and lost lithium responsiveness (LiR). The "set-point" for the ratio of pCRMP2: CRMP2 is elevated uniquely in hiPSC-derived neurons from LiR BPD patients, but not with other psychiatric (including lithium-nonresponsive BPD) and neurological disorders. Lithium (and other pathway modulators) lowers pCRMP2, increasing spine area and density. Human BPD brains show similarly elevated ratios and diminished spine densities; lithium therapy normalizes the ratios and spines. Consistent with such "spine-opathies," human LiR BPD neurons with abnormal ratios evince abnormally steep slopes for calcium flux; lithium normalizes both. Behaviorally, transgenic mice that reproduce lithium's postulated site-of-action in dephosphorylating CRMP2 emulate LiR in BPD. These data suggest that the " lithium response pathway" in BPD governs CRMP2's phosphorylation, which regulates cytoskeletal organization, particularly in spines, modulating neural networks. Aberrations in the posttranslational regulation of this developmentally critical molecule may underlie LiR BPD pathogenesis. Instructively, examining the proteomic profile in hiPSCs of a functional agent-even one whose mechanism-of-action is unknown-might reveal otherwise inscrutable intracellular pathogenic pathways.

sted, utgiver, år, opplag, sider
Washington DC, USA: National Academy of Sciences, 2017
Emneord
posttranslational modification; proteomics; psychiatric disease modeling; CRMP2; dendrites
HSV kategori
Forskningsprogram
Medicin; Molekylär medicin (genetik och patologi); Biomedicin
Identifikatorer
urn:nbn:se:oru:diva-57888 (URN)10.1073/pnas.1700111114 (DOI)000402296700020 ()28500272 (PubMedID)2-s2.0-85020051123 (Scopus ID)
Forskningsfinansiär
NIH (National Institute of Health), R01MH087823
Merknad

Funding Agencies:

NIH's Library of Integrated Network-based Cellular Signatures Program  

Viterbi Foundation Neuroscience Initiative  

Stanley Medical Research Institute  R21MH093958  R33MH087896  R01MH095088 

Tau Consortium  

California Institute of Regenerative Medicine training grants  

University of California, San Diego T32 training grant in psychiatry  

California Bipolar Foundation  

International Bipolar Foundation  

Creation of Innovation Centers for Advanced Interdisciplinary Research Areas Program in the Project for Developing Innovation Systems from the Ministry of Education, Science, Sports and Culture in Japan  42890001   

RC2MH090011 

Tilgjengelig fra: 2017-06-03 Laget: 2017-06-03 Sist oppdatert: 2018-07-31bibliografisk kontrollert
Vumma, R., Johansson, J. & Venizelos, N. (2017). Proinflammatory Cytokines and Oxidative Stress Decrease the Transport of Dopamine Precursor Tyrosine in Human Fibroblasts. Neuropsychobiology, 75(4), 178-184
Åpne denne publikasjonen i ny fane eller vindu >>Proinflammatory Cytokines and Oxidative Stress Decrease the Transport of Dopamine Precursor Tyrosine in Human Fibroblasts
2017 (engelsk)Inngår i: Neuropsychobiology, ISSN 0302-282X, E-ISSN 1423-0224, Vol. 75, nr 4, s. 178-184Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

BACKGROUND: Proinflammatory cytokines and oxidative stress responses have been extensively implicated in the pathophysiology of neuropsychiatric disorders over the past 2 decades. Moreover, disturbed transport of the dopamine precursor (i.e., the amino acid tyrosine) has been demonstrated, in different studies, across fibroblast cell membranes obtained from neuropsychiatric patients. However, the role and influences of proinflammatory cytokines and oxidative stress, and the reasons for disturbed tyrosine transport in neuropsychiatric disorders, are still not evaluated.

AIMS: The present study aimed to assess the role of proinflammatory cytokines and oxidative stress, indicated in many neuropsychiatric disorders, in tyrosine transportation, by using human skin-derived fibroblasts.

METHODS: Fibroblasts obtained from a healthy control were used in this study. Fibroblasts were treated with proinflammatory cytokines (IL-1β, IFN-γ, IL-6, TNF-α), their combinations, and oxidative stress, optimized for concentrations and incubation time, to analyze the uptake of 14C-tyrosine compared to untreated controls.

RESULTS AND CONCLUSION: This study demonstrates that proinflammatory cytokines and oxidative stress decrease the transport of tyrosine (47% and 33%, respectively), which can alter dopamine synthesis. The functionality of the tyrosine transporter could be a new potential biomarker to target for discovering new drugs to counteract the effects of proinflammatory cytokines and oxidative stress in the pathophysiology of neuropsychiatric disorders.

sted, utgiver, år, opplag, sider
Basel: S. Karger, 2017
Emneord
Proinflammatory cytokines; Oxidative stress; Tyrosine transport; Dopamine precursor; Human fibroblasts; Neuropsychiatric disorders
HSV kategori
Identifikatorer
urn:nbn:se:oru:diva-64505 (URN)10.1159/000485130 (DOI)000431062500004 ()29339668 (PubMedID)2-s2.0-85040740113 (Scopus ID)
Forskningsfinansiär
Swedish Research Council, K2007-62X-08318-20-3
Merknad

Funding Agency:

Ingrid Thuring Foundation 

Tilgjengelig fra: 2018-01-25 Laget: 2018-01-25 Sist oppdatert: 2018-08-20bibliografisk kontrollert
Ahmad, A., Venizelos, N. & Hahn-Strömberg, V. (2016). Prognostic Effect of Vascular Endothelial Growth Factor +936C/T Polymorphism on Tumor Growth Pattern and Survival in Patients Diagnosed with Colon Carcinoma. Journal of Tumor Research, 2(1), 1-6, Article ID 1000108.
Åpne denne publikasjonen i ny fane eller vindu >>Prognostic Effect of Vascular Endothelial Growth Factor +936C/T Polymorphism on Tumor Growth Pattern and Survival in Patients Diagnosed with Colon Carcinoma
2016 (engelsk)Inngår i: Journal of Tumor Research, Vol. 2, nr 1, s. 1-6, artikkel-id 1000108Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Introduction: Vascular endothelial growth factor (VEGF) is considered as endothelial cell-specific mitogen that plays an important role in the process of angiogenesis, thereby affecting the prognosis of tumor as angiogenesis is a crucial phase in tumor growth and metastasis. Accordingly, we carried out a case-control study to assess whether VEGF rs3025039 polymorphism affects the growth pattern and susceptibility to colon carcinoma.

Materials and methods: One hundred and fifty, formalin fixed paraffin embedded (FFPE) tissue samples from patients diagnosed with colon carcinoma and the same number of blood controls were used in the present study. VEGF +936 C>T (rs3025039) polymorphism was evaluated by pyrosequencing. Computer image analysis was used to analyse the growth pattern of the colon carcinoma tumor by using cytokeratin-8 stained slides.

Results: A heterozygous genotype TC in rs3025039 polymorphism was found as a significantly protective genotype as compared to homozygous genotypes (CC and TT). However we found no significant correlation between investigated polymorphisms, tumor growth pattern, 5 years survival and other clinicopathological parameters.

Conclusion: We concluded that the heterogenous genotype of VEGF rs3025039 polymorphism appears to be a protective factor for colon carcinoma that could be a useful marker in follow-up studies and may be a genetic determinant for colon carcinoma.

sted, utgiver, år, opplag, sider
OMICS International, 2016
Emneord
Cell specific mitogen; Angiogenesis; Complexity index
HSV kategori
Forskningsprogram
Onkologi; Medicin
Identifikatorer
urn:nbn:se:oru:diva-55032 (URN)
Merknad

The DOI hasn't been activated. Yet.

Tilgjengelig fra: 2017-06-03 Laget: 2017-06-03 Sist oppdatert: 2019-04-10bibliografisk kontrollert
Logotheti, M., Pilalis, E., Venizelos, N., Kolisis, F. & Chatziioannou, A. (2016). Studying Microarray Gene Expression Data of Schizophrenic Patients for Derivation of a Diagnostic Signature through the Aid of Machine Learning. Biometrics & Biostatistics International Journal, 4(5), Article ID 00106.
Åpne denne publikasjonen i ny fane eller vindu >>Studying Microarray Gene Expression Data of Schizophrenic Patients for Derivation of a Diagnostic Signature through the Aid of Machine Learning
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2016 (engelsk)Inngår i: Biometrics & Biostatistics International Journal, ISSN 2378-315X, Vol. 4, nr 5, artikkel-id 00106Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Schizophrenia is a complex psychiatric disease that is affected by multiple genes, some of which could be used as biomarkers for specific diagnosis of the disease. In this work, we explore the power of machine learning methodologies for predicting schizophrenia, through the derivation of a biomarker gene signature for robust diagnostic classification purposes. Postmortem brain gene expression data from the anterior prefrontal cortex of schizophrenia patients were used as training data for the construction of the classifiers. Several machine learning algorithms, such as support vector machines, random forests, and extremely randomized trees classifiers were developed and their performance was tested. After applying the feature selection method of support vector machines recursive feature elimination a 21-gene model was derived. Using these genes for developing classification models, the random forests algorithm outperformed all examined algorithms achieving an area under the curve of 0.98 and sensitivity of 0.89, discriminating schizophrenia from healthy control samples with high efficiency. The 21-gene model that was derived from the feature selection is suggested for classifying schizophrenic patients, as it was successfully applied on an independent dataset of postmortem brain samples from the superior temporal cortex, and resulted in a classification model that achieved an area under the curve score of 0.91. Additionally, the functional analysis of the statistically significant genes indicated many mechanisms related to the immune system.

sted, utgiver, år, opplag, sider
MedCrave, 2016
Emneord
Classification, Schizophrenia, Machine learning, Gene expression, Microarray studies, Support vector machines, Adaboost
HSV kategori
Forskningsprogram
Biomedicin
Identifikatorer
urn:nbn:se:oru:diva-53536 (URN)
Merknad

DOI 10.15406/bbij.2016.04.00106

Tilgjengelig fra: 2016-11-17 Laget: 2016-11-17 Sist oppdatert: 2018-04-27bibliografisk kontrollert
Venizelos, N. & Venizelos, F. (2015). Availability Of Tyrosine And Tryptophan, Precursors Of Dopamine And Serotonin And Neuropsychiatric Disorders: A Review. In: Constantin Soldatos, Dimitris Dikeos, Pedro Ruiz, Dinesh Bhugna, Michelle Riba (Ed.), Pluralism in psychiatry: II. Multidimensional conciderations (pp. 49-54). Bologna, Italy: Medimond
Åpne denne publikasjonen i ny fane eller vindu >>Availability Of Tyrosine And Tryptophan, Precursors Of Dopamine And Serotonin And Neuropsychiatric Disorders: A Review
2015 (engelsk)Inngår i: Pluralism in psychiatry: II. Multidimensional conciderations / [ed] Constantin Soldatos, Dimitris Dikeos, Pedro Ruiz, Dinesh Bhugna, Michelle Riba, Bologna, Italy: Medimond, 2015, s. 49-54Kapittel i bok, del av antologi (Fagfellevurdert)
Abstract [en]

The large neutral amino acids tyrosine and tryptophan are precursors of the neurotransmitters dopamine and serotonin and their availability in the brain may influence neurotransmission. Disturbed neurotransmitter systems, such as the dopaminergic, noradrenergic and serotoninergic systems are implicated in the pathogenesis of neuropsychiatric disorders, including schizophrenia, bipolar disorder, autism and attention deficit hyperactivity disorder (ADHD).

The primary aim of this study is to outline the findings/evidence from different investigations in vitro, concerning aberrant amino acid (tyrosine, tryptophan and alanine) transport in fibroblasts obtained from patients with schizophrenia and their relatives, bipolar-I disorder, autism and ADHD disorders.

The outlines of the findings presented in this study provide evidence that amino acids, tyrosine and tryptophan are strongly involved in schizophrenia, bipolar disorder, autism and ADHD.

sted, utgiver, år, opplag, sider
Bologna, Italy: Medimond, 2015
Emneord
Tyrosine, tryptophan, Alanine transport, Schizophrenia, bipolar disorders, autism, ADHD, Fibroblast
HSV kategori
Forskningsprogram
Biomedicin; Medicin; Psykiatri
Identifikatorer
urn:nbn:se:oru:diva-47708 (URN)000367949700010 ()978-88-7587-722-4 (ISBN)
Tilgjengelig fra: 2016-01-20 Laget: 2016-01-20 Sist oppdatert: 2018-07-02bibliografisk kontrollert
Logotheti, M., Papadodima, O., Chatziioannou, A., Venizelos, N. & Kolisis, F. (2015). Gene Expression Analysis of Fibroblasts from Patients with Bipolar Disorder. Journal of Neuropsychopharmacology & Mental Health, 1(1), 1-9, Article ID 1000103.
Åpne denne publikasjonen i ny fane eller vindu >>Gene Expression Analysis of Fibroblasts from Patients with Bipolar Disorder
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2015 (engelsk)Inngår i: Journal of Neuropsychopharmacology & Mental Health, ISSN 2472-095X, Vol. 1, nr 1, s. 1-9, artikkel-id 1000103Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Bipolar disorder is a severe, lifelong psychiatric disease. The main underlying pathophysiology of the disease is still incomprehensible. Various studies have suggested that many genes of small impact in combination with environmental factors contribute to the expression of the disease. In this study comparative transcriptomic profiling to characterize skin fibroblasts’ gene expression of bipolar disorder patients compared to healthy controls has been performed. Skin fibroblast cells from bipolar disorder patients (n=10) and marched healthy controls (n=5) have been cultured. RNA was extracted and then hybridized onto Illumina Human HT-12 v4 Expression BeadChips. Differentially expressed genes between bipolar disorder samples and healthy controls were identified by performing unequal t-test on log 2 transformed expression values. The resulting gene list was obtained by setting the p-value threshold to 0.05 and by removing genes that presented a fold change ≥ |0.5| (in log 2 scale). We concluded to 457 differentially expressed genes. Among them 127 showed an upregulation and 330 were downregulated. Τhe expression alterations of selected genes were validated by quantitative real-time polymerase chain reaction. In order to derive better insight into the biological mechanisms related to the differentially expressed genes, the lists of significant genes were subjected to pathway analysis and target prioritization indicating various processes such as calcium ion homeostasis, positive regulation of apoptotic process and cellular response to retinoic acid.

sted, utgiver, år, opplag, sider
OMICS International, 2015
Emneord
Skin fibroblasts, Bbipolar disorder, transcriptome, psychiatric diseases, pathway analysis, microarrays
HSV kategori
Forskningsprogram
Psykiatri; Molekylär medicin (genetik och patologi); Biomedicin
Identifikatorer
urn:nbn:se:oru:diva-47705 (URN)10.4172/jnpmh.1000103 (DOI)
Tilgjengelig fra: 2016-01-20 Laget: 2016-01-20 Sist oppdatert: 2018-07-02bibliografisk kontrollert
Westman, O., Larsson, M., Venizelos, N., Hollert, H. & Engwall, M. (2014). An oxygenated metabolite of benzo[a]pyrene increases hepatic beta-oxidation of fatty acids in chick embryos. Environmental science and pollution research international, 21(9), 6243-6251
Åpne denne publikasjonen i ny fane eller vindu >>An oxygenated metabolite of benzo[a]pyrene increases hepatic beta-oxidation of fatty acids in chick embryos
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2014 (engelsk)Inngår i: Environmental science and pollution research international, ISSN 0944-1344, E-ISSN 1614-7499, Vol. 21, nr 9, s. 6243-6251Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Polycyclic aromatic hydrocarbons (PAHs) are well-known carcinogens to humans and ecotoxicological effects have been shown in several studies. However, PAHs can also be oxidized into more water soluble-oxygenated metabolites (Oxy-PAHs). The first purpose of the present project was to (1) assess the effects of a mixture containing three parent PAHs: anthracene, benz[a]anthracene, and benzo[a]pyrene versus a mixture of their oxygenated metabolites, namely: anthracene-9,10-dione, benz[a]anthracene-7,12-dione, and 9,10-dihydrobenzo[a]pyrene-7-(8H)-one on the hepatic fatty acid beta-oxidation in chicken embryos (Gallus gallus domesticus) exposed in ovo. The second and also main purpose of the project was to (2) assess the effects of the parent PAHs versus their oxy-PAHs analogues when injected individually, followed by (3) additional testing of the individual oxy-PAHs. The hepatic beta-oxidation was measured using a tritium release assay with [9,10-H-3]-palmitic acid (16:0) as substrate. The result from the first part (1) showed reduced hepatic beta-oxidation after exposure in ovo to a mixture of three PAHs, however, increased after exposure to the mixture of three oxy-PAHs compared to control. The result from the second part (2) and also the follow-up experiment (3) showed that 9,10-dihydrobenzo[a]pyrene-7-(8H)-one was the causative oxy-PAH. The implication of this finding on the risk assessment of PAH metabolite exposure in avian wildlife remains to be determined. To the best of our knowledge, no similar studies have been reported.

sted, utgiver, år, opplag, sider
Heidelberg: Springer Berlin/Heidelberg, 2014
Emneord
Polycyclic aromatic hydrocarbons, Oxygenated derivatives, Chick embryo, beta-oxidation
HSV kategori
Forskningsprogram
Biologi; Miljövetenskap
Identifikatorer
urn:nbn:se:oru:diva-35205 (URN)10.1007/s11356-013-2471-6 (DOI)000334684700049 ()24385188 (PubMedID)
Merknad

Funding Agency:

Swedish Knowledge Foundation (Stiftelsen for Kunskaps- och Kompetensutveckling)

Tilgjengelig fra: 2014-06-03 Laget: 2014-06-02 Sist oppdatert: 2017-12-05bibliografisk kontrollert
Organisasjoner
Identifikatorer
ORCID-id: ORCID iD iconorcid.org/0000-0001-8102-1804