Transcription of DNA-Methyltransferases in Endothelial Cells Exposed to Mitomycin C
DNA-methyltransferases catalyze DNA methylation in the CpG sites, which play an important role in the maintenance of genome stability. The association between DNA methylation and genotoxic stress resulting in the action of various clastogens has been shown. Genotoxic stress is one of the triggers of...
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| Veröffentlicht in: | Molecular biology (New York) 2022-06, Vol.56 (3), p.437-442 |
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| creator | Sinitsky, M. Yu Sinitskaya, A. V. Shishkova, D. K. Kutikhin, A. G. Minina, V. I. Ponasenko, A. V. |
| description | DNA-methyltransferases catalyze DNA methylation in the CpG sites, which play an important role in the maintenance of genome stability. The association between DNA methylation and genotoxic stress resulting in the action of various clastogens has been shown. Genotoxic stress is one of the triggers of endothelial dysfunction. In this study, the transcription of
DNMT1
,
DNMT3A
and
DNMT3B
genes in coronary (HCAEC) and internal thoracic (HITAEC) artery endothelial cells exposed to alkylating mutagen mitomycin C was studied using quantitative polymerase chain reaction. In HCAEC exposed to mitomycin C,
DNMT1
transcription is 1.7-fold higher compared to the unexposed control. After elimination of the mutagen from the cultures followed by 24-hours of cultivation, a 2-fold increase of transcription of
DNMT3B
in HCAEC exposed to mitomycin C compared to the control was observed. At the same time, no changes in transcription of the studied DNA-methyltransferases were found in HITAEC exposed to the mutagen. Thus, increased transcription of DNA-methyltransferase may be a possible molecular mechanism underlying endothelial dysfunction in response to mutagenic load in an in vitro experiment. |
| doi_str_mv | 10.1134/S0026893322030128 |
| format | Article |
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DNMT1
,
DNMT3A
and
DNMT3B
genes in coronary (HCAEC) and internal thoracic (HITAEC) artery endothelial cells exposed to alkylating mutagen mitomycin C was studied using quantitative polymerase chain reaction. In HCAEC exposed to mitomycin C,
DNMT1
transcription is 1.7-fold higher compared to the unexposed control. After elimination of the mutagen from the cultures followed by 24-hours of cultivation, a 2-fold increase of transcription of
DNMT3B
in HCAEC exposed to mitomycin C compared to the control was observed. At the same time, no changes in transcription of the studied DNA-methyltransferases were found in HITAEC exposed to the mutagen. Thus, increased transcription of DNA-methyltransferase may be a possible molecular mechanism underlying endothelial dysfunction in response to mutagenic load in an in vitro experiment.</description><identifier>ISSN: 0026-8933</identifier><identifier>EISSN: 1608-3245</identifier><identifier>DOI: 10.1134/S0026893322030128</identifier><language>eng</language><publisher>Moscow: Pleiades Publishing</publisher><subject>Biochemistry ; Biomedical and Life Sciences ; CpG islands ; DNA methylation ; DNA methyltransferase ; DNMT1 protein ; Endothelial cells ; Genomes ; Genotoxicity ; Human Genetics ; Life Sciences ; Mitomycin C ; Molecular Cell Biology ; Thorax ; Transcription</subject><ispartof>Molecular biology (New York), 2022-06, Vol.56 (3), p.437-442</ispartof><rights>Pleiades Publishing, Inc. 2022. ISSN 0026-8933, Molecular Biology, 2022, Vol. 56, No. 3, pp. 437–442. © Pleiades Publishing, Inc., 2022. Russian Text © The Author(s), 2022, published in Molekulyarnaya Biologiya, 2022, Vol. 56, No. 3, pp. 491–497.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c198t-3616c06499d62945540c5b1cd187c53236c65c0c77b13e0c8038412ab0a117243</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1134/S0026893322030128$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1134/S0026893322030128$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Sinitsky, M. Yu</creatorcontrib><creatorcontrib>Sinitskaya, A. V.</creatorcontrib><creatorcontrib>Shishkova, D. K.</creatorcontrib><creatorcontrib>Kutikhin, A. G.</creatorcontrib><creatorcontrib>Minina, V. I.</creatorcontrib><creatorcontrib>Ponasenko, A. V.</creatorcontrib><title>Transcription of DNA-Methyltransferases in Endothelial Cells Exposed to Mitomycin C</title><title>Molecular biology (New York)</title><addtitle>Mol Biol</addtitle><description>DNA-methyltransferases catalyze DNA methylation in the CpG sites, which play an important role in the maintenance of genome stability. The association between DNA methylation and genotoxic stress resulting in the action of various clastogens has been shown. Genotoxic stress is one of the triggers of endothelial dysfunction. In this study, the transcription of
DNMT1
,
DNMT3A
and
DNMT3B
genes in coronary (HCAEC) and internal thoracic (HITAEC) artery endothelial cells exposed to alkylating mutagen mitomycin C was studied using quantitative polymerase chain reaction. In HCAEC exposed to mitomycin C,
DNMT1
transcription is 1.7-fold higher compared to the unexposed control. After elimination of the mutagen from the cultures followed by 24-hours of cultivation, a 2-fold increase of transcription of
DNMT3B
in HCAEC exposed to mitomycin C compared to the control was observed. At the same time, no changes in transcription of the studied DNA-methyltransferases were found in HITAEC exposed to the mutagen. Thus, increased transcription of DNA-methyltransferase may be a possible molecular mechanism underlying endothelial dysfunction in response to mutagenic load in an in vitro experiment.</description><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>CpG islands</subject><subject>DNA methylation</subject><subject>DNA methyltransferase</subject><subject>DNMT1 protein</subject><subject>Endothelial cells</subject><subject>Genomes</subject><subject>Genotoxicity</subject><subject>Human Genetics</subject><subject>Life Sciences</subject><subject>Mitomycin C</subject><subject>Molecular Cell Biology</subject><subject>Thorax</subject><subject>Transcription</subject><issn>0026-8933</issn><issn>1608-3245</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><recordid>eNp1kF9LwzAUxYMoOKcfwLeAz9V7kzRNH0edf2Dqw-ZzydLUdXRNTTJw396WCT6IcOE8nN85Fw4h1wi3iFzcLQGYVDnnjAEHZOqETFCCSjgT6SmZjHYy-ufkIoQtAA7HJmS58roLxjd9bFxHXU3vX2fJi42bQxtHq7ZeBxto09F5V7m4sW2jW1rYtg10_tW7YCsaHX1potsdzIAVl-Ss1m2wVz86Je8P81XxlCzeHp-L2SIxmKuYcInSgBR5XkmWizQVYNI1mgpVZlLOuDQyNWCybI3cglHAlUCm16ARMyb4lNwce3vvPvc2xHLr9r4bXpZMZhxASJ4NFB4p410I3tZl75ud9ocSoRy3K_9sN2TYMRMGtvuw_rf5_9A3wU9uJQ</recordid><startdate>20220601</startdate><enddate>20220601</enddate><creator>Sinitsky, M. Yu</creator><creator>Sinitskaya, A. V.</creator><creator>Shishkova, D. K.</creator><creator>Kutikhin, A. G.</creator><creator>Minina, V. I.</creator><creator>Ponasenko, A. V.</creator><general>Pleiades Publishing</general><general>Springer Nature B.V</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope></search><sort><creationdate>20220601</creationdate><title>Transcription of DNA-Methyltransferases in Endothelial Cells Exposed to Mitomycin C</title><author>Sinitsky, M. Yu ; Sinitskaya, A. V. ; Shishkova, D. K. ; Kutikhin, A. G. ; Minina, V. I. ; Ponasenko, A. 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V.</creatorcontrib><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><jtitle>Molecular biology (New York)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sinitsky, M. Yu</au><au>Sinitskaya, A. V.</au><au>Shishkova, D. K.</au><au>Kutikhin, A. G.</au><au>Minina, V. I.</au><au>Ponasenko, A. V.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Transcription of DNA-Methyltransferases in Endothelial Cells Exposed to Mitomycin C</atitle><jtitle>Molecular biology (New York)</jtitle><stitle>Mol Biol</stitle><date>2022-06-01</date><risdate>2022</risdate><volume>56</volume><issue>3</issue><spage>437</spage><epage>442</epage><pages>437-442</pages><issn>0026-8933</issn><eissn>1608-3245</eissn><abstract>DNA-methyltransferases catalyze DNA methylation in the CpG sites, which play an important role in the maintenance of genome stability. The association between DNA methylation and genotoxic stress resulting in the action of various clastogens has been shown. Genotoxic stress is one of the triggers of endothelial dysfunction. In this study, the transcription of
DNMT1
,
DNMT3A
and
DNMT3B
genes in coronary (HCAEC) and internal thoracic (HITAEC) artery endothelial cells exposed to alkylating mutagen mitomycin C was studied using quantitative polymerase chain reaction. In HCAEC exposed to mitomycin C,
DNMT1
transcription is 1.7-fold higher compared to the unexposed control. After elimination of the mutagen from the cultures followed by 24-hours of cultivation, a 2-fold increase of transcription of
DNMT3B
in HCAEC exposed to mitomycin C compared to the control was observed. At the same time, no changes in transcription of the studied DNA-methyltransferases were found in HITAEC exposed to the mutagen. Thus, increased transcription of DNA-methyltransferase may be a possible molecular mechanism underlying endothelial dysfunction in response to mutagenic load in an in vitro experiment.</abstract><cop>Moscow</cop><pub>Pleiades Publishing</pub><doi>10.1134/S0026893322030128</doi><tpages>6</tpages></addata></record> |
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| subjects | Biochemistry Biomedical and Life Sciences CpG islands DNA methylation DNA methyltransferase DNMT1 protein Endothelial cells Genomes Genotoxicity Human Genetics Life Sciences Mitomycin C Molecular Cell Biology Thorax Transcription |
| title | Transcription of DNA-Methyltransferases in Endothelial Cells Exposed to Mitomycin C |
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