Journal
INTERNATIONAL HEART JOURNAL
Volume 52, Issue 6, Pages 382-387Publisher
INT HEART JOURNAL ASSOC
DOI: 10.1536/ihj.52.382
Keywords
Regulatory T cells; Myocardial ischemia; Cytokine
Categories
Funding
- Takeda Science Foundation
- Suzuken Memorial Foundation
- Research Foundation for Pharmaceutical Sciences
- Japan Society for the Promotion of Science (JSPS)
Ask authors/readers for more resources
Downregulation of CD4+CD25+ regulatory T lymphocytes (Treg) has been found in local atherosclerotic lesions and in patients with myocardial infarction (MI). However, the roles of Treg in MI and the following inflammatory response have not yet been well elucidated. Therefore, we hypothesized that adoptive transfer of Treg could attenuate the postinfarction inflammatory response protecting from adverse remodeling, and we attempted to elucidate the mechanism of delayed heart failure after MI. To clarify the role of Treg in MI, we used a murine MI model and administered a single intravenous injection of Treg (1 x 10(5)) (treatment, 17 = 6) or saline (control, n = 7) and sacrificed the mice on day 14. Echocardiograms revealed that Treg improved LV contraction after MI. Histopathology also showed that Treg negated MI-induced LV remodeling. RT-PCR demonstrated that the mRNA levels of IFN-gamma in hearts were lower and Foxp3 in spleens were higher in the treatment group than in the control group. We observed that adoptive Treg transfer could attenuate MI-induced cardiac remodeling through the IFN-gamma and Foxp3 alteration. (Int Heart J 2011; 52: 382-387)
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available