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In response to DNA damage, BRCA2 participates in homology\u2010directed DNA damage repair to maintain genome stability. Genome\u2010wide association studies have identified an association between BRCA2 single nucleotide polymorphisms and plasma\u2010lipid levels and lipid deregulation in humans. To date, DNA damage, apoptosis, and lipid deregulation are recognized as central pathways for endothelial dysfunction and atherosclerosis; however, the role of BRCA2 in endothelial dysfunction remains to be elucidated. To determine the role of BRCA2 in endothelial dysfunction,\n                    <jats:italic>BRCA2<\/jats:italic>\n                    was silenced in human umbilical vein endothelial cells (ECs) and assessed for markers of DNA damage, apoptosis, and endothelial function following oxidized low\u2010density lipoprotein (oxLDL) treatment. OxLDL was found to induce significant reactive oxygen species (ROS) production in\n                    <jats:italic>BRCA2<\/jats:italic>\n                    \u2010silenced ECs. This increase in ROS production was associated with exacerbated DNA damage evidenced by increased expression and activation of DNA double\u2010stranded break (DSB) marker \u03b3H2AX and reduced RAD51\u2010foci formation\u2014an essential regulator of DSB repair. Increased DSBs were associated with enhanced expression and activation of pro\u2010apoptotic p53 and significant apoptosis in oxLDL\u2010treated\n                    <jats:italic>BRCA2<\/jats:italic>\n                    \u2010silenced ECs. Loss of BRCA2 in ECs was further associated with oxLDL\u2010induced impaired tube\u2010forming potential and eNOS expression. Collectively, the data reveals, for the first time, a novel role of BRCA2 as a regulator of EC survival and function in the setting of oxLDL treatment\n                    <jats:italic>in vitro<\/jats:italic>\n                    . Additionally, the data provide important clues regarding the potential susceptibility of BRCA2 mutation carriers to endothelial dysfunction, atherosclerosis, and other cardiovascular diseases.\n                  <\/jats:p>","DOI":"10.14814\/phy2.14481","type":"journal-article","created":{"date-parts":[[2020,7,8]],"date-time":"2020-07-08T01:35:53Z","timestamp":1594172153000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":26,"title":["EXPRESSION OF CONCERN: BReast CAncer susceptibility gene 2 deficiency exacerbates oxidized LDL\u2010induced DNA damage and endothelial apoptosis"],"prefix":"10.14814","volume":"8","author":[{"given":"Shweta","family":"Singh","sequence":"first","affiliation":[{"name":"Department of Medical Biophysics Schulich School of Medicine and Dentistry University of Western Ontario London ON 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N.","family":"Matkar","sequence":"additional","affiliation":[{"name":"Division of Cardiology Keenan Research Centre for Biomedical Science and Li Ka Shing Knowledge Institute of St. Michael's Hospital Toronto ON Canada"},{"name":"Institute of Medical Science University of Toronto Toronto ON Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zongyi","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Medical Biophysics Schulich School of Medicine and Dentistry University of Western Ontario London ON Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lilian","family":"Esene","sequence":"additional","affiliation":[{"name":"Department of Medical Biophysics Schulich School of Medicine and Dentistry University of Western Ontario London ON Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"Adam","sequence":"additional","affiliation":[{"name":"Division of Cardiology Keenan Research Centre 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