resident cardiac immune cells and expression of the ectonucleotidase enzymes cd39 and cd73 after ischemic injury居民的心脏免疫细胞和表达ectonucleotidase酶cd39和cd73后缺血性损伤.pdfVIP
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resident cardiac immune cells and expression of the ectonucleotidase enzymes cd39 and cd73 after ischemic injury居民的心脏免疫细胞和表达ectonucleotidase酶cd39和cd73后缺血性损伤
Resident Cardiac Immune Cells and Expression of the
Ectonucleotidase Enzymes CD39 and CD73 after Ischemic
Injury
¨ . . ¨
Florian Bonner , Nadine Borg , Sandra Burghoff, Jurgen Schrader*
¨ ¨
Department of Molecular Cardiology, Heinrich-Heine-University Dusseldorf, Dusseldorf, Germany
Abstract
Background: The ectoenzymes CD39 and CD73 are expressed by a broad range of immune cells and promote the
extracellular degradation of nucleotides to anti-inflammatory adenosine. This study explored the abundance of CD73 and
CD39 on circulating and resident cardiac leukocytes and coronary endothelial cells under control conditions and in response
to inflammation following myocardial ischemia and reperfusion (I/R).
Methods and Results: A method was elaborated to permit FACS analysis of non-myocardial cells (resident leukocytes,
coronary endothelium and CD312 CD452 cells) of the unstressed heart. Under control conditions the murine heart
contained 2.3 6103 resident leukocytes/mg tissue, the most prominent fraction being antigen-presenting mononuclear cells
(CD11b+ + + +
CD11c F4/80 MHCII ) followed by B-cells, monocytes and T-cells. CD73 was highly expressed on circulating and
resident cardiac lymphoid cells with little expression on myeloid cells, while the opposite was true for CD39.
Cardiomyocytes and erythrocytes do not measurably express CD39/CD73 and CD39 dominates on coronary endothelium.
Three days after I/R, CD73 was significantly upregulated on invading granulocytes (2.8-fold) and T-cells (1.5-fold). Compared
with coronary endothelia
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