TRECKシステムを用いた、心血管疾患におけるミエロイド系細胞集団の機能解析法の構築

  • 横田 洸成
    大阪大・院薬・臨床薬効解析学分野
  • 冨松 聖史
    大阪大・院薬・臨床薬効解析学分野
  • 小南 春祐
    大阪大・院薬・臨床薬効解析学分野
  • 梶浦 僚太
    大阪大・院薬・臨床薬効解析学分野
  • 田中 翔大
    大阪大・院薬・臨床薬効解析学分野
  • 尾花 理徳
    大阪大・院薬・臨床薬効解析学分野 大阪大・先導的学際研究機構生命医科学融合フロンティア研究部
  • 岡田 欣晃
    大阪大・院薬・臨床薬効解析学分野
  • 藤尾 慈
    大阪大・院薬・臨床薬効解析学分野 大阪大・先導的学際研究機構生命医科学融合フロンティア研究部

書誌事項

タイトル別名
  • Establishment of a novel method for analysis of biological functions of myeloid cell subpopulation in cardiovascular diseases using TRECK system.

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<p>[Background]Though the importance of myeloid cells in the cardiac remodeling after myocardial infarction (MI) is widely accepted, it remains to be fully elucidated how myeloid cells regulate post-infarct inflammation, at least partially, because subpopulation-specific cell knock-out methods are not available.</p><p>[Methods and Results]We generated transgenic mice expressing diphtheria toxin receptor (DTR)/GFP fusion protein under the control of CD11b promoter in a Cre recombinase-expressing cell-specific manner (CD11b-DTR TG mice). Double TG mice (DTG mice) were generated by crossing CD11b-DTR TG mice with LysM-Cre mice that express Cre recombinase preferentially in monocytes/macrophages. The MI model was created in DTG mice by ligation of the left anterior descending branch. Flow cytometry analysis revealed that monocytes were labeled with GFP in the peripheral blood 4 days after MI. Consistently, immunofluorescent microscopic analysis showed that GFP⁺ cells infiltrated into the infarcted heart. Importantly, the administration of diphtheria toxin resulted in the depletion of GFP⁺ cells in peripheral blood and post-infarct myocardium. </p><p>[Conclusion]CD11b-DTR TG mice are useful for labeling and/or depleting subpopulation of myeloid cells in MI model.</p>

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