Chronic irradiation of human cells reduces histone levels and deregulates gene expression
Identifieur interne : 000187 ( an2020/Analysis ); précédent : 000186; suivant : 000188Chronic irradiation of human cells reduces histone levels and deregulates gene expression
Auteurs : Donna J. Lowe ; Mareike Herzog ; Thorsten Mosler [Allemagne] ; Howard Cohen ; Sarah Felton ; Petra Beli [Allemagne] ; Ken Raj ; Yaron Galanty ; Stephen P. JacksonSource :
- Scientific Reports [ 2045-2322 ] ; 2020.
Abstract
Over the past decades, there have been huge advances in understanding cellular responses to ionising radiation (IR) and DNA damage. These studies, however, were mostly executed with cell lines and mice using single or multiple acute doses of radiation. Hence, relatively little is known about how continuous exposure to low dose ionising radiation affects normal cells and organisms, even though our cells are constantly exposed to low levels of radiation. We addressed this issue by examining the consequences of exposing human primary cells to continuous ionising γ-radiation delivered at 6–20 mGy/h. Although these dose rates are estimated to inflict fewer than a single DNA double-strand break (DSB) per hour per cell, they still caused dose-dependent reductions in cell proliferation and increased cellular senescence. We concomitantly observed histone protein levels to reduce by up to 40%, which in contrast to previous observations, was not mainly due to protein degradation but instead correlated with reduced histone gene expression. Histone reductions were accompanied by enlarged nuclear size paralleled by an increase in global transcription, including that of pro-inflammatory genes. Thus, chronic irradiation, even at low dose-rates, can induce cell senescence and alter gene expression via a hitherto uncharacterised epigenetic route. These features of chronic radiation represent a new aspect of radiation biology.
Url:
DOI: 10.1038/s41598-020-59163-4
PubMed: 32042076
PubMed Central: 7010678
Affiliations:
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Lowe</name><affiliation><nlm:aff id="Aff1"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 5909 016X</institution-id><institution-id institution-id-type="GRID">grid.271308.f</institution-id><institution>Radiation Effects Department, Centre for Radiation,</institution><institution>Chemical and Environmental Hazards, Public Health England, Chilton,</institution></institution-wrap>Didcot, Oxfordshire OX11 0RQ UK</nlm:aff><wicri:noCountry code="subfield">Oxfordshire OX11 0RQ UK</wicri:noCountry></affiliation><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000000121885934</institution-id><institution-id institution-id-type="GRID">grid.5335.0</institution-id><institution>Wellcome/Cancer Research UK Gurdon Institute and Department of Biochemistry,</institution><institution>University of Cambridge,</institution></institution-wrap>Cambridge, CB2 1QN UK</nlm:aff><wicri:noCountry code="subfield">CB2 1QN UK</wicri:noCountry></affiliation></author><author><name sortKey="Herzog, Mareike" sort="Herzog, Mareike" uniqKey="Herzog M" first="Mareike" last="Herzog">Mareike Herzog</name><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000000121885934</institution-id><institution-id institution-id-type="GRID">grid.5335.0</institution-id><institution>Wellcome/Cancer Research UK Gurdon Institute and Department of Biochemistry,</institution><institution>University of Cambridge,</institution></institution-wrap>Cambridge, CB2 1QN UK</nlm:aff><wicri:noCountry code="subfield">CB2 1QN UK</wicri:noCountry></affiliation></author><author><name sortKey="Mosler, Thorsten" sort="Mosler, Thorsten" uniqKey="Mosler T" first="Thorsten" last="Mosler">Thorsten Mosler</name><affiliation wicri:level="1"><nlm:aff id="Aff3"><institution-wrap><institution-id institution-id-type="ISNI">0000 0004 1794 1771</institution-id><institution-id 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UK</wicri:noCountry></affiliation></author><author><name sortKey="Jackson, Stephen P" sort="Jackson, Stephen P" uniqKey="Jackson S" first="Stephen P." last="Jackson">Stephen P. Jackson</name><affiliation><nlm:aff id="Aff2"><institution-wrap><institution-id institution-id-type="ISNI">0000000121885934</institution-id><institution-id institution-id-type="GRID">grid.5335.0</institution-id><institution>Wellcome/Cancer Research UK Gurdon Institute and Department of Biochemistry,</institution><institution>University of Cambridge,</institution></institution-wrap>Cambridge, CB2 1QN UK</nlm:aff><wicri:noCountry code="subfield">CB2 1QN UK</wicri:noCountry></affiliation></author></analytic><series><title level="j">Scientific Reports</title><idno type="eISSN">2045-2322</idno><imprint><date when="2020">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p id="Par1">Over the past decades, there have been huge advances in understanding cellular responses to ionising radiation (IR) and DNA damage. These studies, however, were mostly executed with cell lines and mice using single or multiple acute doses of radiation. Hence, relatively little is known about how continuous exposure to low dose ionising radiation affects normal cells and organisms, even though our cells are constantly exposed to low levels of radiation. We addressed this issue by examining the consequences of exposing human primary cells to continuous ionising γ-radiation delivered at 6–20 mGy/h. Although these dose rates are estimated to inflict fewer than a single DNA double-strand break (DSB) per hour per cell, they still caused dose-dependent reductions in cell proliferation and increased cellular senescence. We concomitantly observed histone protein levels to reduce by up to 40%, which in contrast to previous observations, was not mainly due to protein degradation but instead correlated with reduced histone gene expression. Histone reductions were accompanied by enlarged nuclear size paralleled by an increase in global transcription, including that of pro-inflammatory genes. Thus, chronic irradiation, even at low dose-rates, can induce cell senescence and alter gene expression via a hitherto uncharacterised epigenetic route. These features of chronic radiation represent a new aspect of radiation biology.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Adams, Mj" uniqKey="Adams M">MJ Adams</name></author><author><name sortKey="Hardenbergh, Ph" uniqKey="Hardenbergh P">PH Hardenbergh</name></author><author><name sortKey="Constine, Ls" uniqKey="Constine L">LS Constine</name></author><author><name sortKey="Lipshultz, Se" uniqKey="Lipshultz S">SE Lipshultz</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Shimizu, Y" uniqKey="Shimizu Y">Y Shimizu</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Baker, Je" uniqKey="Baker J">JE Baker</name></author><author><name sortKey="Moulder, Je" uniqKey="Moulder J">JE Moulder</name></author><author><name sortKey="Hopewell, Jw" uniqKey="Hopewell J">JW Hopewell</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Darby, Sc" 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Baker</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bussian, Tj" uniqKey="Bussian T">TJ Bussian</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Waldera Lupa, Dm" uniqKey="Waldera Lupa D">DM Waldera Lupa</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Ozcan, S" uniqKey="Ozcan S">S Ozcan</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vaughan, De" uniqKey="Vaughan D">DE Vaughan</name></author><author><name sortKey="Rai, R" uniqKey="Rai R">R Rai</name></author><author><name sortKey="Khan, Ss" uniqKey="Khan S">SS Khan</name></author><author><name sortKey="Eren, M" uniqKey="Eren M">M Eren</name></author><author><name sortKey="Ghosh, Ak" uniqKey="Ghosh A">AK Ghosh</name></author></analytic></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Allemagne</li></country></list><tree><noCountry><name sortKey="Cohen, Howard" sort="Cohen, Howard" uniqKey="Cohen H" first="Howard" last="Cohen">Howard Cohen</name><name sortKey="Felton, Sarah" sort="Felton, Sarah" uniqKey="Felton S" first="Sarah" last="Felton">Sarah Felton</name><name sortKey="Galanty, Yaron" sort="Galanty, Yaron" uniqKey="Galanty Y" first="Yaron" last="Galanty">Yaron Galanty</name><name sortKey="Herzog, Mareike" sort="Herzog, Mareike" uniqKey="Herzog M" first="Mareike" last="Herzog">Mareike Herzog</name><name sortKey="Jackson, Stephen P" sort="Jackson, Stephen P" uniqKey="Jackson S" first="Stephen P." last="Jackson">Stephen P. Jackson</name><name sortKey="Lowe, Donna J" sort="Lowe, Donna J" uniqKey="Lowe D" first="Donna J." last="Lowe">Donna J. Lowe</name><name sortKey="Raj, Ken" sort="Raj, Ken" uniqKey="Raj K" first="Ken" last="Raj">Ken Raj</name></noCountry><country name="Allemagne"><noRegion><name sortKey="Mosler, Thorsten" sort="Mosler, Thorsten" uniqKey="Mosler T" first="Thorsten" last="Mosler">Thorsten Mosler</name></noRegion><name sortKey="Beli, Petra" sort="Beli, Petra" uniqKey="Beli P" first="Petra" last="Beli">Petra Beli</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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