［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.

［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.

［Conclusion］CD11b-DTR TG mice are useful for labeling and/or depleting subpopulation of myeloid cells in MI model.