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Article ; Online: In-Utero Low-Dose Irradiation Leads to Persistent Alterations in the Mouse Heart Proteome.

Bakshi, Mayur V / Azimzadeh, Omid / Merl-Pham, Juliane / Verreet, Tine / Hauck, Stefanie M / Benotmane, Mohammed A / Atkinson, Michael J / Tapio, Soile

PloS one

2016 Volume 11, Issue 6, Page(s) e0156952

Abstract: Prenatal exposure to stress such as increased level of reactive oxygen species or antiviral therapy are known factors leading to adult heart defects. The risks following a radiation exposure during fetal period are unknown, as are the mechanisms of any ... ...

Abstract	Prenatal exposure to stress such as increased level of reactive oxygen species or antiviral therapy are known factors leading to adult heart defects. The risks following a radiation exposure during fetal period are unknown, as are the mechanisms of any potential cardiac damage. The aim of this study was to gather evidence for possible damage by investigating long-term changes in the mouse heart proteome after prenatal exposure to low and moderate radiation doses. Pregnant C57Bl/6J mice received on embryonic day 11 (E11) a single total body dose of ionizing radiation that ranged from 0.02 Gy to 1.0 Gy. The offspring were sacrificed at the age of 6 months or 2 years. Quantitative proteomic analysis of heart tissue was performed using Isotope Coded Protein Label technology and tandem mass spectrometry. The proteomics data were analyzed by bioinformatics and key changes were validated by immunoblotting. Persistent changes were observed in the expression of proteins representing mitochondrial respiratory complexes, redox and heat shock response, and the cytoskeleton, even at the low dose of 0.1 Gy. The level of total and active form of the kinase MAP4K4 that is essential for the embryonic development of mouse heart was persistently decreased at the radiation dose of 1.0 Gy. This study provides the first insight into the molecular mechanisms of cardiac impairment induced by ionizing radiation exposure during the prenatal period.
MeSH term(s)	Animals ; Female ; Male ; Maternal Exposure/adverse effects ; Mice ; Muscle Proteins/biosynthesis ; Myocardium/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects/metabolism ; Proteome/biosynthesis ; Radiation Injuries, Experimental/metabolism ; X-Rays/adverse effects
Chemical Substances	Muscle Proteins ; Proteome
Language	English
Publishing date	2016-06-08
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0156952
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Integrative Proteomics and Targeted Transcriptomics Analyses in Cardiac Endothelial Cells Unravel Mechanisms of Long-Term Radiation-Induced Vascular Dysfunction

Azimzadeh, Omid / Atkinson Michael J / Bakshi Mayur V / Janik Dirk / Merl-Pham Juliane / Multhoff Gabriele / Sarioglu Hakan / Sievert Wolfgang / Tapio Soile / Ueffing Marius / Yentrapalli Ramesh

Journal of Proteome Research. 2015 Feb. 06, v. 14, no. 2

2015

Abstract: Epidemiological data from radiotherapy patients show the damaging effect of ionizing radiation on heart and vasculature. The endothelium is the main target of radiation damage and contributes essentially to the development of cardiac injury. However, the ...

Abstract	Epidemiological data from radiotherapy patients show the damaging effect of ionizing radiation on heart and vasculature. The endothelium is the main target of radiation damage and contributes essentially to the development of cardiac injury. However, the molecular mechanisms behind the radiation-induced endothelial dysfunction are not fully understood. In the present study, 10-week-old C57Bl/6 mice received local X-ray heart doses of 8 or 16 Gy and were sacrificed after 16 weeks; the controls were sham-irradiated. The cardiac microvascular endothelial cells were isolated from the heart tissue using streptavidin-CD31-coated microbeads. The cells were lysed and proteins were labeled with duplex isotope-coded protein label methodology for quantification. All samples were analyzed by LCâESIâMS/MS and Proteome Discoverer software. The proteomics data were further studied by bioinformatics tools and validated by targeted transcriptomics, immunoblotting, immunohistochemistry, and serum profiling. Radiation-induced endothelial dysfunction was characterized by impaired energy metabolism and perturbation of the insulin/IGF-PI3K-Akt signaling pathway. The data also strongly suggested premature endothelial senescence, increased oxidative stress, decreased NO availability, and enhanced inflammation as main causes of radiation-induced long-term vascular dysfunction. Detailed data on molecular mechanisms of radiation-induced vascular injury as compiled here are essential in developing radiotherapy strategies that minimize cardiovascular complications.
Keywords	bioinformatics ; blood serum ; computer software ; endothelial cells ; endothelium ; energy metabolism ; heart ; immunoblotting ; immunohistochemistry ; inflammation ; mice ; microbeads ; nitric oxide ; oxidative stress ; patients ; proteins ; proteome ; proteomics ; radiotherapy ; signal transduction ; transcriptomics ; X-radiation
Language	English
Dates of publication	2015-0206
Size	p. 1203-1219.
Publishing place	American Chemical Society
Document type	Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021%2Fpr501141b
Database	NAL-Catalogue (AGRICOLA)

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Article: Total Body Exposure to Low-Dose Ionizing Radiation Induces Long-Term Alterations to the Liver Proteome of Neonatally Exposed Mice

Bakshi, Mayur V / Atkinson Michael J / Azimzadeh Omid / Barjaktarovic Zarko / Buratovic Sonja / Eriksson Per / Hauck Stefanie M / Kempf Stefan J / Merl-Pham Juliane / Tapio Soile

Journal of Proteome Research. 2015 Jan. 02, v. 14, no. 1

2015

Abstract: Tens of thousands of people are being exposed daily to environmental low-dose gamma radiation. Epidemiological data indicate that such low radiation doses may negatively affect liver function and result in the development of liver disease. However, the ... ...

Abstract	Tens of thousands of people are being exposed daily to environmental low-dose gamma radiation. Epidemiological data indicate that such low radiation doses may negatively affect liver function and result in the development of liver disease. However, the biological mechanisms behind these adverse effects are unknown. The aim of this study was to investigate radiation-induced damage in the liver after low radiation doses. Neonatal male NMRI mice were exposed to total body irradiation on postnatal day 10 using acute single doses ranging from 0.02 to 1.0 Gy. Early (1 day) and late (7 months) changes in the liver proteome were tracked using isotope-coded protein label technology and quantitative mass spectrometry. Our data indicate that low and moderate radiation doses induce an immediate inhibition of the glycolysis pathway and pyruvate dehydrogenase availability in the liver. Furthermore, they lead to significant long-term alterations in lipid metabolism and increased liver inflammation accompanying inactivation of the transcription factor peroxisome proliferator-activated receptor alpha. This study contributes to the understanding of the potential risk of liver damage in populations environmentally exposed to ionizing radiation.
Keywords	adverse effects ; gamma radiation ; glycolysis ; inflammation ; ionization ; irradiation ; lipid metabolism ; liver ; liver diseases ; liver function ; males ; mass spectrometry ; mice ; peroxisome proliferator-activated receptors ; proteome ; pyruvate dehydrogenase (lipoamide) ; risk
Language	English
Dates of publication	2015-0102
Size	p. 366-373.
Publishing place	American Chemical Society
Document type	Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021%2Fpr500890n
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: A dose-dependent perturbation in cardiac energy metabolism is linked to radiation-induced ischemic heart disease in Mayak nuclear workers.

Azimzadeh, Omid / Azizova, Tamara / Merl-Pham, Juliane / Subramanian, Vikram / Bakshi, Mayur V / Moseeva, Maria / Zubkova, Olga / Hauck, Stefanie M / Anastasov, Nataša / Atkinson, Michael J / Tapio, Soile

Oncotarget

2017 Volume 8, Issue 6, Page(s) 9067–9078

Abstract: Epidemiological studies show a significant increase in ischemic heart disease (IHD) incidence associated with total external gamma-ray dose among Mayak plutonium enrichment plant workers. Our previous studies using mouse models suggest that persistent ... ...

Abstract	Epidemiological studies show a significant increase in ischemic heart disease (IHD) incidence associated with total external gamma-ray dose among Mayak plutonium enrichment plant workers. Our previous studies using mouse models suggest that persistent alteration of heart metabolism due to the inhibition of peroxisome proliferator-activated receptor (PPAR) alpha accompanies cardiac damage after high doses of ionising radiation. The aim of the present study was to elucidate the mechanism of radiation-induced IHD in humans. The cardiac proteome response to irradiation was analysed in Mayak workers who were exposed only to external doses of gamma rays. All participants were diagnosed during their lifetime with IHD that also was the cause of death. Label-free quantitative proteomics analysis was performed on tissue samples from the cardiac left ventricles of individuals stratified into four radiation dose groups (0 Gy, < 100 mGy, 100-500 mGy, and > 500 mGy). The groups could be separated using principal component analysis based on all proteomics features. Proteome profiling showed a dose-dependent increase in the number of downregulated mitochondrial and structural proteins. Both proteomics and immunoblotting showed decreased expression of several oxidative stress responsive proteins in the irradiated hearts. The phosphorylation of transcription factor PPAR alpha was increased in a dose-dependent manner, which is indicative of a reduction in transcriptional activity with increased radiation dose. These data suggest that chronic external radiation enhances the risk for IHD by inhibiting PPAR alpha and altering the expression of mitochondrial, structural, and antioxidant components of the heart.
Language	English
Publishing date	2017-02-07
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.10424
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Differential Impact of Single-Dose Fe Ion and X-Ray Irradiation on Endothelial Cell Transcriptomic and Proteomic Responses.

Baselet, Bjorn / Azimzadeh, Omid / Erbeldinger, Nadine / Bakshi, Mayur V / Dettmering, Till / Janssen, Ann / Ktitareva, Svetlana / Lowe, Donna J / Michaux, Arlette / Quintens, Roel / Raj, Kenneth / Durante, Marco / Fournier, Claudia / Benotmane, Mohammed A / Baatout, Sarah / Sonveaux, Pierre / Tapio, Soile / Aerts, An

Frontiers in pharmacology

2017 Volume 8, Page(s) 570

Abstract: Background and Purpose: ...

Abstract	Background and Purpose:
Language	English
Publishing date	2017-09-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587355-6
ISSN	1663-9812
ISSN	1663-9812
DOI	10.3389/fphar.2017.00570
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Article ; Online: Integrative proteomics and targeted transcriptomics analyses in cardiac endothelial cells unravel mechanisms of long-term radiation-induced vascular dysfunction.

Azimzadeh, Omid / Sievert, Wolfgang / Sarioglu, Hakan / Merl-Pham, Juliane / Yentrapalli, Ramesh / Bakshi, Mayur V / Janik, Dirk / Ueffing, Marius / Atkinson, Michael J / Multhoff, Gabriele / Tapio, Soile

Journal of proteome research

2015 Volume 14, Issue 2, Page(s) 1203–1219

Abstract	Epidemiological data from radiotherapy patients show the damaging effect of ionizing radiation on heart and vasculature. The endothelium is the main target of radiation damage and contributes essentially to the development of cardiac injury. However, the molecular mechanisms behind the radiation-induced endothelial dysfunction are not fully understood. In the present study, 10-week-old C57Bl/6 mice received local X-ray heart doses of 8 or 16 Gy and were sacrificed after 16 weeks; the controls were sham-irradiated. The cardiac microvascular endothelial cells were isolated from the heart tissue using streptavidin-CD31-coated microbeads. The cells were lysed and proteins were labeled with duplex isotope-coded protein label methodology for quantification. All samples were analyzed by LC-ESI-MS/MS and Proteome Discoverer software. The proteomics data were further studied by bioinformatics tools and validated by targeted transcriptomics, immunoblotting, immunohistochemistry, and serum profiling. Radiation-induced endothelial dysfunction was characterized by impaired energy metabolism and perturbation of the insulin/IGF-PI3K-Akt signaling pathway. The data also strongly suggested premature endothelial senescence, increased oxidative stress, decreased NO availability, and enhanced inflammation as main causes of radiation-induced long-term vascular dysfunction. Detailed data on molecular mechanisms of radiation-induced vascular injury as compiled here are essential in developing radiotherapy strategies that minimize cardiovascular complications.
MeSH term(s)	Animals ; Blood Vessels/cytology ; Blood Vessels/physiopathology ; Blood Vessels/radiation effects ; Chromatography, Liquid ; Gene Expression Profiling ; Mice ; Mice, Inbred C57BL ; Proteomics ; Spectrometry, Mass, Electrospray Ionization ; Tandem Mass Spectrometry ; Transcriptome
Language	English
Publishing date	2015-02-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/pr501141b
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Total body exposure to low-dose ionizing radiation induces long-term alterations to the liver proteome of neonatally exposed mice.

Bakshi, Mayur V / Azimzadeh, Omid / Barjaktarovic, Zarko / Kempf, Stefan J / Merl-Pham, Juliane / Hauck, Stefanie M / Buratovic, Sonja / Eriksson, Per / Atkinson, Michael J / Tapio, Soile

Journal of proteome research

2015 Volume 14, Issue 1, Page(s) 366–373

Abstract	Tens of thousands of people are being exposed daily to environmental low-dose gamma radiation. Epidemiological data indicate that such low radiation doses may negatively affect liver function and result in the development of liver disease. However, the biological mechanisms behind these adverse effects are unknown. The aim of this study was to investigate radiation-induced damage in the liver after low radiation doses. Neonatal male NMRI mice were exposed to total body irradiation on postnatal day 10 using acute single doses ranging from 0.02 to 1.0 Gy. Early (1 day) and late (7 months) changes in the liver proteome were tracked using isotope-coded protein label technology and quantitative mass spectrometry. Our data indicate that low and moderate radiation doses induce an immediate inhibition of the glycolysis pathway and pyruvate dehydrogenase availability in the liver. Furthermore, they lead to significant long-term alterations in lipid metabolism and increased liver inflammation accompanying inactivation of the transcription factor peroxisome proliferator-activated receptor alpha. This study contributes to the understanding of the potential risk of liver damage in populations environmentally exposed to ionizing radiation.
MeSH term(s)	Animals ; Animals, Newborn/metabolism ; Computational Biology ; Dose-Response Relationship, Radiation ; Immunoblotting ; Lipid Metabolism/radiation effects ; Liver/metabolism ; Liver/radiation effects ; Male ; Mice ; Proteome/metabolism ; Proteome/radiation effects ; Proteomics ; Radiation, Ionizing ; Tandem Mass Spectrometry ; Whole-Body Irradiation/adverse effects
Chemical Substances	Proteome
Language	English
Publishing date	2015-01-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	2078618-9
ISSN	1535-3907 ; 1535-3893
ISSN (online)	1535-3907
ISSN	1535-3893
DOI	10.1021/pr500890n
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Long-term effects of acute low-dose ionizing radiation on the neonatal mouse heart: a proteomic study.

Bakshi, Mayur V / Barjaktarovic, Zarko / Azimzadeh, Omid / Kempf, Stefan J / Merl, Juliane / Hauck, Stefanie M / Eriksson, Per / Buratovic, Sonja / Atkinson, Michael J / Tapio, Soile

Radiation and environmental biophysics

2013 Volume 52, Issue 4, Page(s) 451–461

Abstract: Epidemiological studies establish that children and young adults are especially susceptible to radiation-induced cardiovascular disease (CVD). The biological mechanisms behind the elevated CVD risk following exposure at young age remain unknown. The ... ...

Abstract	Epidemiological studies establish that children and young adults are especially susceptible to radiation-induced cardiovascular disease (CVD). The biological mechanisms behind the elevated CVD risk following exposure at young age remain unknown. The present study aims to elucidate the long-term effects of ionizing radiation by studying the murine cardiac proteome after exposure to low and moderate radiation doses. NMRI mice received single doses of total body (60)Co gamma-irradiation on postnatal day 10 and were sacrificed 7 months later. Changes in cardiac protein expression were quantified using isotope-coded protein label and tandem mass spectrometry. We identified 32, 31, 66, and 34 significantly deregulated proteins after doses of 0.02, 0.1, 0.5, and 1.0 Gy, respectively. The four doses shared 9 deregulated proteins. Bioinformatics analysis showed that most of the deregulated proteins belonged to a limited set of biological categories, including metabolic processes, inflammatory response, and cytoskeletal structure. The transcription factor peroxisome proliferator-activated receptor alpha was predicted as a common upstream regulator of several deregulated proteins. This study indicates that both adaptive and maladaptive responses to the initial radiation damage persist well into adulthood. It will contribute to the understanding of the long-term consequences of radiation-induced injury and developmental alterations in the neonatal heart.
MeSH term(s)	Animals ; Animals, Newborn ; Dose-Response Relationship, Radiation ; Gene Ontology ; Heart/radiation effects ; Male ; Mice ; Myocardium/metabolism ; Protein Interaction Maps/radiation effects ; Proteomics ; Signal Transduction/radiation effects ; Time Factors ; Whole-Body Irradiation
Language	English
Publishing date	2013-07-24
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	124987-3
ISSN	1432-2099 ; 0301-634X
ISSN (online)	1432-2099
ISSN	0301-634X
DOI	10.1007/s00411-013-0483-8
Database	MEDical Literature Analysis and Retrieval System OnLINE

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