Low-dose aspirin protective effects are correlated with deregulation of HNF factor expression in the preeclamptic placentas from mice and humans
Aspirin (acetyl-salicylic acid) is one of the most ancient drugs of the human pharmacopeia. Nonetheless, its action at low doses is not well understood at the molecular level. One of the applications of low-dose aspirin treatment is the prevention of preeclampsia (PE) in patients at risk. Foeto-plac...
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| Veröffentlicht in: | Cell death discovery 2019-05, Vol.5 (1), p.94, Article 94 |
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| description | Aspirin (acetyl-salicylic acid) is one of the most ancient drugs of the human pharmacopeia. Nonetheless, its action at low doses is not well understood at the molecular level. One of the applications of low-dose aspirin treatment is the prevention of preeclampsia (PE) in patients at risk. Foeto-placental overexpression of the STOX1A transcription factor in mice triggers PE symptoms. Transcriptomic analysis of the placentas, showed that aspirin massively down-regulates genes of the coagulation and complement cascade, as well as genes involved in lipid transport. The genes modified by aspirin treatment are not the ones that are modified by STOX1 overexpression, suggesting that aspirin could act downstream, symptomatically on the preeclamptic disease. Bioinformatics analysis of the promoters of the deregulated genes showed that they are strongly enriched in HNF transcription factors-binding sites, in accordance with existing literature showing their roles as regulators of coagulation. Two of these transcription factors,
Hnf1β
and
Hnf4α
are found down-regulated by aspirin treatment. In parallel, we show that in human patient placentas, aspirin-induced deregulations of genes of the coagulation cascade are also observed. Finally, the expression of Hnf1β target sequences (
Kif12
,
F2
,
Hnf4α
promoters and a synthetic concatemer of the Hnf1β-binding site) were investigated by transfection in trophoblast cell models, with or without aspirin treatment and with or without STOX1A overexpression. In this model we observed that STOX1A and aspirin tended to synergize in the down-regulation of Hnf1β target genes in trophoblasts. |
| doi_str_mv | 10.1038/s41420-019-0170-x |
| format | Article |
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Hnf1β
and
Hnf4α
are found down-regulated by aspirin treatment. In parallel, we show that in human patient placentas, aspirin-induced deregulations of genes of the coagulation cascade are also observed. Finally, the expression of Hnf1β target sequences (
Kif12
,
F2
,
Hnf4α
promoters and a synthetic concatemer of the Hnf1β-binding site) were investigated by transfection in trophoblast cell models, with or without aspirin treatment and with or without STOX1A overexpression. In this model we observed that STOX1A and aspirin tended to synergize in the down-regulation of Hnf1β target genes in trophoblasts.</description><identifier>ISSN: 2058-7716</identifier><identifier>EISSN: 2058-7716</identifier><identifier>DOI: 10.1038/s41420-019-0170-x</identifier><identifier>PMID: 31098302</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/337/2019 ; 631/443/592 ; Apoptosis ; Aspirin ; Binding sites ; Biochemistry ; Bioinformatics ; Biomedical and Life Sciences ; Cell Biology ; Cell culture ; Cell Cycle Analysis ; Coagulation ; Gene regulation ; Life Sciences ; Placenta ; Pre-eclampsia ; Preeclampsia ; Promoters ; Reproductive Biology ; Salicylic acid ; Sexual reproduction ; Stem Cells ; Synergism ; Transcription factors ; Transfection ; Trophoblasts</subject><ispartof>Cell death discovery, 2019-05, Vol.5 (1), p.94, Article 94</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Attribution</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c504t-ec587ef5e869b4b45eff582c01786a0f3350b0defb4049cb4fae82d165346f393</citedby><cites>FETCH-LOGICAL-c504t-ec587ef5e869b4b45eff582c01786a0f3350b0defb4049cb4fae82d165346f393</cites><orcidid>0000-0002-1915-0717 ; 0000-0003-4623-0584</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6510804/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6510804/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31098302$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-02349216$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>Ducat, Aurélien</creatorcontrib><creatorcontrib>Vargas, Alexandra</creatorcontrib><creatorcontrib>Doridot, Ludivine</creatorcontrib><creatorcontrib>Bagattin, Alessia</creatorcontrib><creatorcontrib>Lerner, Jonathan</creatorcontrib><creatorcontrib>Vilotte, Jean-Luc</creatorcontrib><creatorcontrib>Buffat, Christophe</creatorcontrib><creatorcontrib>Pontoglio, Marco</creatorcontrib><creatorcontrib>Miralles, Francisco</creatorcontrib><creatorcontrib>Vaiman, Daniel</creatorcontrib><title>Low-dose aspirin protective effects are correlated with deregulation of HNF factor expression in the preeclamptic placentas from mice and humans</title><title>Cell death discovery</title><addtitle>Cell Death Discov</addtitle><addtitle>Cell Death Discov</addtitle><description>Aspirin (acetyl-salicylic acid) is one of the most ancient drugs of the human pharmacopeia. Nonetheless, its action at low doses is not well understood at the molecular level. One of the applications of low-dose aspirin treatment is the prevention of preeclampsia (PE) in patients at risk. Foeto-placental overexpression of the STOX1A transcription factor in mice triggers PE symptoms. Transcriptomic analysis of the placentas, showed that aspirin massively down-regulates genes of the coagulation and complement cascade, as well as genes involved in lipid transport. The genes modified by aspirin treatment are not the ones that are modified by STOX1 overexpression, suggesting that aspirin could act downstream, symptomatically on the preeclamptic disease. Bioinformatics analysis of the promoters of the deregulated genes showed that they are strongly enriched in HNF transcription factors-binding sites, in accordance with existing literature showing their roles as regulators of coagulation. Two of these transcription factors,
Hnf1β
and
Hnf4α
are found down-regulated by aspirin treatment. In parallel, we show that in human patient placentas, aspirin-induced deregulations of genes of the coagulation cascade are also observed. Finally, the expression of Hnf1β target sequences (
Kif12
,
F2
,
Hnf4α
promoters and a synthetic concatemer of the Hnf1β-binding site) were investigated by transfection in trophoblast cell models, with or without aspirin treatment and with or without STOX1A overexpression. In this model we observed that STOX1A and aspirin tended to synergize in the down-regulation of Hnf1β target genes in trophoblasts.</description><subject>631/337/2019</subject><subject>631/443/592</subject><subject>Apoptosis</subject><subject>Aspirin</subject><subject>Binding sites</subject><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biomedical and Life Sciences</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Cell Cycle Analysis</subject><subject>Coagulation</subject><subject>Gene regulation</subject><subject>Life Sciences</subject><subject>Placenta</subject><subject>Pre-eclampsia</subject><subject>Preeclampsia</subject><subject>Promoters</subject><subject>Reproductive Biology</subject><subject>Salicylic acid</subject><subject>Sexual reproduction</subject><subject>Stem Cells</subject><subject>Synergism</subject><subject>Transcription factors</subject><subject>Transfection</subject><subject>Trophoblasts</subject><issn>2058-7716</issn><issn>2058-7716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kk1v1DAQhiMEolXpD-CCLHGBQ2D8lY8LUlVRFmlVLnC2HGe86yqJg51sl3_BT8ZRSlsqcbBszTzzznj0ZtlrCh8o8OpjFFQwyIHW6ZSQH59lpwxklZclLZ4_ep9k5zHeAACVpSgr_jI74RTqigM7zX5v_W3e-ohEx9EFN5Ax-AnN5A5I0Nr0ikQHJMaHgJ2esCW3btqTFgPu5hRwfiDeks31FbHaTD4QPI4BY1wSSW_aY9JENJ3ux8kZMnba4DDpSGzwPemdSc2HluznXg_xVfbC6i7i-d19lv24-vz9cpNvv335enmxzY0EMeVoZFWilVgVdSMaIdOssmImraIqNFjOJTTQom0EiNo0wmqsWEsLyUVhec3Psk-r7jg3PbbLREF3agyu1-GX8tqpfzOD26udP6hCUqhAJIH3q8D-SdnmYquWGDAuakaLA03su7tmwf-cMU6qd9Fg1-kB_RwVY5yBoJzKhL59gt74OQxpFYlirGYSakgUXSkTfIwB7f0EFNRiD7XaQyV7qMUe6phq3jz-8X3FXzMkgK1ATKlhh-Gh9f9V_wB15Mgs</recordid><startdate>20190510</startdate><enddate>20190510</enddate><creator>Ducat, Aurélien</creator><creator>Vargas, Alexandra</creator><creator>Doridot, Ludivine</creator><creator>Bagattin, Alessia</creator><creator>Lerner, Jonathan</creator><creator>Vilotte, Jean-Luc</creator><creator>Buffat, Christophe</creator><creator>Pontoglio, Marco</creator><creator>Miralles, Francisco</creator><creator>Vaiman, Daniel</creator><general>Nature Publishing Group UK</general><general>Springer Nature B.V</general><general>Springer Nature</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-1915-0717</orcidid><orcidid>https://orcid.org/0000-0003-4623-0584</orcidid></search><sort><creationdate>20190510</creationdate><title>Low-dose aspirin protective effects are correlated with deregulation of HNF factor expression in the preeclamptic placentas from mice and humans</title><author>Ducat, Aurélien ; 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Nonetheless, its action at low doses is not well understood at the molecular level. One of the applications of low-dose aspirin treatment is the prevention of preeclampsia (PE) in patients at risk. Foeto-placental overexpression of the STOX1A transcription factor in mice triggers PE symptoms. Transcriptomic analysis of the placentas, showed that aspirin massively down-regulates genes of the coagulation and complement cascade, as well as genes involved in lipid transport. The genes modified by aspirin treatment are not the ones that are modified by STOX1 overexpression, suggesting that aspirin could act downstream, symptomatically on the preeclamptic disease. Bioinformatics analysis of the promoters of the deregulated genes showed that they are strongly enriched in HNF transcription factors-binding sites, in accordance with existing literature showing their roles as regulators of coagulation. Two of these transcription factors,
Hnf1β
and
Hnf4α
are found down-regulated by aspirin treatment. In parallel, we show that in human patient placentas, aspirin-induced deregulations of genes of the coagulation cascade are also observed. Finally, the expression of Hnf1β target sequences (
Kif12
,
F2
,
Hnf4α
promoters and a synthetic concatemer of the Hnf1β-binding site) were investigated by transfection in trophoblast cell models, with or without aspirin treatment and with or without STOX1A overexpression. In this model we observed that STOX1A and aspirin tended to synergize in the down-regulation of Hnf1β target genes in trophoblasts.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31098302</pmid><doi>10.1038/s41420-019-0170-x</doi><orcidid>https://orcid.org/0000-0002-1915-0717</orcidid><orcidid>https://orcid.org/0000-0003-4623-0584</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell death discovery, 2019-05, Vol.5 (1), p.94, Article 94 |
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| subjects | 631/337/2019 631/443/592 Apoptosis Aspirin Binding sites Biochemistry Bioinformatics Biomedical and Life Sciences Cell Biology Cell culture Cell Cycle Analysis Coagulation Gene regulation Life Sciences Placenta Pre-eclampsia Preeclampsia Promoters Reproductive Biology Salicylic acid Sexual reproduction Stem Cells Synergism Transcription factors Transfection Trophoblasts |
| title | Low-dose aspirin protective effects are correlated with deregulation of HNF factor expression in the preeclamptic placentas from mice and humans |
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