Resident Cardiac Immune Cells and Expression of the Ectonucleotidase Enzymes CD39 and CD73 after Ischemic Injury 英文参考文献.docVIP
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Resident Cardiac Immune Cells and Expression of the Ectonucleotidase Enzymes CD39 and CD73 after Ischemic Injury 英文参考文献
ResidentCardiacImmuneCellsandExpressionofthe
EctonucleotidaseEnzymesCD39andCD73afterIschemic
Injury
FlorianBo¨nner.,NadineBorg.,SandraBurghoff,Ju¨rgenSchrader*
DepartmentofMolecularCardiology,Heinrich-Heine-UniversityDu¨sseldorf,Du¨sseldorf,Germany
Abstract
Background: The ectoenzymes CD39 and CD73 are expressed by a broad range of immune cells and promote the
extracellulardegradationofnucleotidestoanti-inflammatoryadenosine.ThisstudyexploredtheabundanceofCD73and
CD39oncirculatingandresidentcardiacleukocytesandcoronaryendothelialcellsundercontrolconditionsandinresponse
toinflammationfollowingmyocardialischemiaandreperfusion(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
contained2.3610 residentleukocytes/mgtissue,themostprominentfractionbeingantigen-presentingmononuclearcells
(CD11b CD11c+F4/80+MHCII+)followedbyB-cells,monocytesandT-cells.CD73washighlyexpressedoncirculatingand
resident cardiac lymphoid cells with little expression on myeloid cells, while the opposite was true for CD39.
CardiomyocytesanderythrocytesdonotmeasurablyexpressCD39/CD73andCD39dominatesoncoronaryendothelium.
ThreedaysafterI/R,CD73wassignificantlyupregulatedoninvadinggranulocytes(2.8-fold)andT-cells(1.5-fold).Compared
withcoronaryendothelialcells,CD73associatedwithleukocytescomprised2/3ofthetotalcardiacCD73.
3
+
Conclusion: Our study suggests that extracellular ATP formed during I/R is preferentially degraded by CD39 present on
myeloidcells,whiletheformationofimmunosuppressiveadenosineismainlycatalysedbyCD73presentongranulocytes
and lymphoid cells. Upregulated CD73 on granulocytes and T-cells infiltrating the injured heart is consistent with the
existenceofanautocrineadenosinergicloopwhichmaypromotethehealingprocess.
Citation:Bo¨nnerF,BorgN,BurghoffS,SchraderJ(2012)ResidentCardiacImmuneCellsandExpressionoft
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