In Utero Low Dose Irradiation Leads to Persistent Alterations in the Mouse Heart Proteome
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In Utero Low Dose Irradiation Leads to Persistent Alterations in the Mouse Heart Proteome. / Bakshi, Mayur V; Azimzadee"h, Omid; Merl-Pham, Juliane; Verreet, Tine; Hauck, Stefanie M; Benotmane, Rafi; Atkinson, Michael J; Tapio, Soile; Baatout, Sarah (Peer reviewer).
In: PLOS ONE, Vol. 11, No. 6, 08.06.2016.Research output: Contribution to journal › Article › peer-review
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T1 - In Utero Low Dose Irradiation Leads to Persistent Alterations in the Mouse Heart Proteome
AU - Bakshi, Mayur V
AU - Azimzadee"h, Omid
AU - Merl-Pham, Juliane
AU - Verreet, Tine
AU - Hauck, Stefanie M
AU - Benotmane, Rafi
AU - Atkinson, Michael J
AU - Tapio, Soile
A2 - Baatout, Sarah
N1 - Score=10
PY - 2016/6/8
Y1 - 2016/6/8
N2 - Prenatal exposure to stress such as increased level of reactive oxygen species or antiviraltherapy are known factors leading to adult heart defects. The risks following a radiationexposure during fetal period are unknown, as are the mechanisms of any potential cardiacdamage. The aim of this study was to gather evidence for possible damage by investigatinglong-term changes in the mouse heart proteome after prenatal exposure to low and moderateradiation doses. Pregnant C57Bl/6J mice received on embryonic day 11 (E11) a singletotal body dose of ionizing radiation that ranged from 0.02 Gy to 1.0 Gy. The offspring weresacrificed at the age of 6 months or 2 years. Quantitative proteomic analysis of heart tissuewas performed using Isotope Coded Protein Label technology and tandem mass spectrometry.The proteomics data were analyzed by bioinformatics and key changes were validatedby immunoblotting. Persistent changes were observed in the expression of proteins representingmitochondrial 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 kinaseMAP4K4 that is essential for the embryonic development of mouse heart was
AB - Prenatal exposure to stress such as increased level of reactive oxygen species or antiviraltherapy are known factors leading to adult heart defects. The risks following a radiationexposure during fetal period are unknown, as are the mechanisms of any potential cardiacdamage. The aim of this study was to gather evidence for possible damage by investigatinglong-term changes in the mouse heart proteome after prenatal exposure to low and moderateradiation doses. Pregnant C57Bl/6J mice received on embryonic day 11 (E11) a singletotal body dose of ionizing radiation that ranged from 0.02 Gy to 1.0 Gy. The offspring weresacrificed at the age of 6 months or 2 years. Quantitative proteomic analysis of heart tissuewas performed using Isotope Coded Protein Label technology and tandem mass spectrometry.The proteomics data were analyzed by bioinformatics and key changes were validatedby immunoblotting. Persistent changes were observed in the expression of proteins representingmitochondrial 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 kinaseMAP4K4 that is essential for the embryonic development of mouse heart was
KW - in utero
KW - heart
KW - proteome
UR - http://ecm.sckcen.be/OTCS/llisapi.dll/open/19600859
U2 - 10.1371/journal.pone.0156952
DO - 10.1371/journal.pone.0156952
M3 - Article
VL - 11
JO - PLOS ONE
JF - PLOS ONE
SN - 1932-6203
IS - 6
ER -
ID: 1452074