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  • 작성자 : 김성수
  • 작성일 : 2015-09-24
  • 조회 : 2,665회

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콜로라도 의대에서 연수하고 현재는 미국 뉴멕시코 의대 마취과에서 레지던트 하고 있는 서 성욱 동문이 콜로라도에서 하던 일이 논문으로 발표되었습니다.
우리 의전원, 의대 학생들도 연구도 하고 공부도 하여 훌륭한 의학자가 되어 주길 바랍니다.


J Immunol. 2015 Aug 15;195(4):1732-43. doi: 10.4049/jimmunol.1402288. Epub 2015 Jul 1.

Differential Tissue-Specific Function of Adora2b in Cardioprotection.

Seo SW1, Koeppen M2, Bonney S3, Gobel M3, Thayer M3, Harter PN4, Ravid K5, Eltzschig HK3, Mittelbronn M4, Walker L6, Eckle T7.

Author information

1. Department of Anesthesiology, University of Colorado Denver, Aurora, CO 80045; Department of Biochemistry and Molecular Biology, School of Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea;
2. Department of Anesthesiology, University of Colorado Denver, Aurora, CO 80045; Department of Anesthesiology, Ludwig Maximilians University Munich, 80336 Munich, Germany;
3. Department of Anesthesiology, University of Colorado Denver, Aurora, CO 80045;
4. Institute of Neurology (Edinger Institute), University of Frankfurt, 60528 Frankfurt, Germany;
5. Department of Medicine, Boston University School of Medicine, Boston, MA 02118; Department of Biochemistry, Boston University School of Medicine, Boston, MA 02118; and.
6. Division of Cardiology, University of Colorado Denver, Aurora, CO 80045.
7. Department of Anesthesiology, University of Colorado Denver, Aurora, CO 80045; tobias.eckle@ucdenver.edu.

Abstract

The adenosine A2b receptor (Adora2b) has been implicated in cardioprotection from myocardial ischemia. As such, Adora2b was found to be critical in ischemic preconditioning (IP) or ischemia/reperfusion (IR) injury of the heart. Whereas Adora2b is present on various cells types, the tissue-specific role of Adora2b in cardioprotection is still unknown. To study the tissue-specific role of Adora2b signaling on inflammatory cells, endothelia, or myocytes during myocardial ischemia in vivo, we intercrossed floxed Adora2b mice with Lyz2-Cre(+), VE-cadherin-Cre(+), or myosin-Cre(+) transgenic mice, respectively. Mice were exposed to 60 min of myocardial ischemia with or without IP (four times for 5 min) followed by 120 min of reperfusion. Cardioprotection by IP was abolished in Adora2b(f/f)-VE-cadherin-Cre(+) or Adora2b(f/f)-myosin-Cre(+), indicating that Adora2b signaling on endothelia or myocytes mediates IP. In contrast, primarily Adora2b signaling on inflammatory cells was necessary to provide cardioprotection in IR injury, indicated by significantly larger infarcts and higher troponin levels in Adora2b(f/f)-Lyz2-Cre(+) mice only. Cytokine profiling of IR injury in Adora2b(f/f)-Lyz2-Cre(+) mice pointed toward polymorphonuclear neutrophils (PMNs). Analysis of PMNs from Adora2b(f/f)-Lyz2-Cre(+) confirmed PMNs as one source of identified tissue cytokines. Finally, adoptive transfer of Adora2b(-/-) PMNs revealed a critical role of Adora2b on PMNs in cardioprotection from IR injury. Adora2b signaling mediates different types of cardioprotection in a tissue-specific manner. These findings have implications for the use of Adora2b agonists in the treatment or prevention of myocardial injury by ischemia.

Copyright © 2015 by The American Association of Immunologists, Inc.

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