Key result
Ccr5-deficient mice receiving allografts showed significantly diminished intragraft mRNA expression of Mmp3, Mmp12, Mmp13, and Adam8, leading to increased allograft survival and reduced remodeling.
Why the study?
Does Ccr5 deficiency reduce intragraft metalloproteinase expression and transplant arteriosclerosis in mice receiving heart and carotid-artery allografts?
Population
Wild-type and Ccr5-deficient mice as recipients of fully MHC-mismatched heart and carotid-artery allografts
Comparison
Ccr5 deficiency (genetic knockout) vs Wild-type mice
Design
Preclinical
Follow-up
2 and 6 days for gene expression
Authors
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Ccr5 targeting may limit murine allograft remodeling; leaves open translation to human transplant arteriosclerosis.
Does Ccr5 deficiency reduce intragraft metalloproteinase expression and transplant arteriosclerosis in mice receiving heart and carotid-artery allografts?
Ccr5 deficiency reduces early tissue remodeling and metalloproteinase expression, leading to improved allograft survival and reduced transplant arteriosclerosis in a murine model.
Luckow et al. (2004) studied Allograft rejection and transplant arteriosclerosis. Ccr5 deficiency vs. Wild-type was evaluated on Intragraft mRNA expression of metalloproteinase genes and allograft survival. Ccr5-deficient mice receiving allografts showed significantly diminished intragraft mRNA expression of Mmp3, Mmp12, Mmp13, and Adam8, leading to increased allograft survival and reduced remodeling.
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