Gender disparity in LDL-induced cardiovascular damage and the protective role of estrogens against electronegative LDL

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• 作者：An-Sheng Lee (10) (11) (15) (16)
  Wei-Yu Chen (11)
  Hua-Chen Chan (11) (14)
  Jing-Fang Hsu (11)
  Ming-Yi Shen (10) (11)
  Chia-Ming Chang (11)
  Henry Bair (12)
  Ming-Jai Su (13)
  Kuan-Cheng Chang (10) (16)
  Chu-Huang Chen (10) (11) (14) (15) (16)
  
• 关键词：Electronegative low ; density lipoprotein ; Metabolic syndrome ; Cardiovascular disease ; Aortic senescence ; 17β ; estradiol ; Genistein
• 刊名：Cardiovascular Diabetology
• 出版年：2014
• 出版时间：December 2014
• 年：2014
• 卷：13
• 期：1
• 全文大小：913 KB
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• 作者单位：An-Sheng Lee (10) (11) (15) (16)
  Wei-Yu Chen (11)
  Hua-Chen Chan (11) (14)
  Jing-Fang Hsu (11)
  Ming-Yi Shen (10) (11)
  Chia-Ming Chang (11)
  Henry Bair (12)
  Ming-Jai Su (13)
  Kuan-Cheng Chang (10) (16)
  Chu-Huang Chen (10) (11) (14) (15) (16)
  
  10. Graduate Institute of Clinical Medical Science, China Medical University, Taichung, Taiwan
  11. L5 Research Center, China Medical University Hospital, Taichung, Taiwan
  15. Vascular and Medicinal Research, Texas Heart Institute, 6770 Bertner Avenue, MC 2-255, Houston, TX, 77030, USA
  16. Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
  14. Center for Lipid Biosciences and Department of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
  12. George R. Brown School of Engineering, Rice University, Houston, Texas, USA
  13. Graduate Institute of Pharmacology, National Taiwan University, Taipei, Taiwan
  
• ISSN：1475-2840

文摘

Background Increased levels of the most electronegative type of LDL, L5, have been observed in the plasma of patients with metabolic syndrome (MetS) and ST-segment elevation myocardial infarction and can induce endothelial dysfunction. Because men have a higher predisposition to developing coronary artery disease than do premenopausal women, we hypothesized that LDL electronegativity is increased in men and promotes endothelial damage. Methods L5 levels were compared between middle-aged men and age-matched, premenopausal women with or without MetS. We further studied the effects of gender-influenced LDL electronegativity on aortic cellular senescence and DNA damage in leptin receptor–deficient (db/db) mice by using senescence-associated–οgalactosidase and γH2AX staining, respectively. We also studied the protective effects of 17β-estradiol and genistein against electronegative LDL–induced senescence in cultured bovine aortic endothelial cells (BAECs). Results L5 levels were higher in MetS patients than in healthy subjects (P <-.001), particularly in men (P =-.001). LDL isolated from male db/db mice was more electronegative than that from male or female wild-type mice. In addition, LDL from male db/db mice contained abundantly more apolipoprotein CIII and induced more BAEC senescence than did female db/db or wild-type LDL. In the aortas of db/db mice but not wild-type mice, we observed cellular senescence and DNA damage, and the effect was more significant in male than in female db/db mice. Pretreatment with 17β-estradiol or genistein inhibited BAEC senescence induced by male or female db/db LDL and downregulated the expression of lectin-like oxidized LDL receptor-1 and tumor necrosis factor-alpha protein. Conclusion The gender dichotomy of LDL-induced cardiovascular damage may underlie the increased propensity to coronary artery disease in men.