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Adenosine Formed by CD73 on T Cells Inhibits Cardiac Inflammation and Fibrosis and Preserves Contractile Function in Transverse Aortic Constriction-Induced Heart Failure.

Abstract Structural damage during heart failure development leads to increased infiltration of leukocytes. Because purinergic signaling on immune cells may impact on the inflammatory response, we evaluated the role of ecto-5'-nucleotidase (CD73) on the development of heart failure after transverse aortic constriction (TAC) using global and T-cell-specific CD73(-)(/-) mice.
PMID
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Authors

Mayor MeshTerms
Keywords

5′-nucleotidase

collagen

heart failure

inflammation

receptors, purinergic P1

Journal Title circulation. heart failure
Publication Year Start




PMID- 28404626
OWN - NLM
STAT- MEDLINE
DA  - 20170413
DCOM- 20170418
LR  - 20170418
IS  - 1941-3297 (Electronic)
IS  - 1941-3289 (Linking)
VI  - 10
IP  - 4
DP  - 2017 Apr
TI  - Adenosine Formed by CD73 on T Cells Inhibits Cardiac Inflammation and Fibrosis
      and Preserves Contractile Function in Transverse Aortic Constriction-Induced
      Heart Failure.
LID - e003346 [pii]
LID - 10.1161/CIRCHEARTFAILURE.116.003346 [doi]
AB  - BACKGROUND: Structural damage during heart failure development leads to increased
      infiltration of leukocytes. Because purinergic signaling on immune cells may
      impact on the inflammatory response, we evaluated the role of
      ecto-5'-nucleotidase (CD73) on the development of heart failure after transverse 
      aortic constriction (TAC) using global and T-cell-specific CD73-/- mice. METHODS 
      AND RESULTS: Leukocytes infiltrating the failing heart were analyzed by a
      multistep enzymatic procedure over a period of 16 weeks using
      fluorescence-activated cell sorting. TAC significantly enhanced the infiltration 
      of leukocytes, especially T cells. The fraction of CD73 expressing cells
      increased over time exclusively on cytotoxic T cells, T-helper cells, and
      regulatory T cells. Cardiac function significantly declined in T-cell-specific
      CD4-Cre+/-CD73flox/flox mice identical to that observed in global CD73 mutants
      and was associated with enhanced fibrosis (collagen, laminin, vimentin,
      periostin). Expression analysis by quantitative reverse transcription polymerase 
      chain reaction of extracellular purine degrading enzymes and P1 and P2 receptors 
      on T cells isolated from the injured heart revealed profound upregulation of the 
      enzymatic machinery for hydrolysis of extracellular adenosine triphosphate and
      nicotinamide adenine dinucleotide, both pathways converging in the formation of
      AMP and adenosine via CD73. Among the P1 receptors, only the A2a receptor was
      significantly upregulated after TAC. T cells isolated from TAC-treated hearts
      show enhanced production of proinflammatory cytokines (interleukin-3,
      interleukin-6, interleukin-13, interleukin-17, macrophage inflammatory
      proteins-1alpha, and macrophage inflammatory proteins-1beta) when CD73 was
      lacking. CONCLUSIONS: Our data provide first evidence that CD73 on T cells plays 
      an important anti-inflammatory role in TAC-induced heart failure, which is
      associated with antifibrotic activity and reduced production of proinflammatory
      cytokines most likely by activation of the adenosine A2a receptor.
CI  - (c) 2017 American Heart Association, Inc.
FAU - Quast, Christine
AU  - Quast C
AD  - From the Division of Cardiology, Pulmonary Diseases and Vascular Medicine (C.Q.) 
      and Department of Molecular Cardiology (C.Q., C.A., Z.D., N.B., J.S.), University
      Hospital Dusseldorf, Heinrich-Heine-University Dusseldorf, Germany.
FAU - Alter, Christina
AU  - Alter C
AD  - From the Division of Cardiology, Pulmonary Diseases and Vascular Medicine (C.Q.) 
      and Department of Molecular Cardiology (C.Q., C.A., Z.D., N.B., J.S.), University
      Hospital Dusseldorf, Heinrich-Heine-University Dusseldorf, Germany.
FAU - Ding, Zhaoping
AU  - Ding Z
AD  - From the Division of Cardiology, Pulmonary Diseases and Vascular Medicine (C.Q.) 
      and Department of Molecular Cardiology (C.Q., C.A., Z.D., N.B., J.S.), University
      Hospital Dusseldorf, Heinrich-Heine-University Dusseldorf, Germany.
FAU - Borg, Nadine
AU  - Borg N
AD  - From the Division of Cardiology, Pulmonary Diseases and Vascular Medicine (C.Q.) 
      and Department of Molecular Cardiology (C.Q., C.A., Z.D., N.B., J.S.), University
      Hospital Dusseldorf, Heinrich-Heine-University Dusseldorf, Germany.
FAU - Schrader, Jurgen
AU  - Schrader J
AD  - From the Division of Cardiology, Pulmonary Diseases and Vascular Medicine (C.Q.) 
      and Department of Molecular Cardiology (C.Q., C.A., Z.D., N.B., J.S.), University
      Hospital Dusseldorf, Heinrich-Heine-University Dusseldorf, Germany.
      [email protected]
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Circ Heart Fail
JT  - Circulation. Heart failure
JID - 101479941
RN  - 0 (Interleukin-3)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
RN  - 9007-34-5 (Collagen)
RN  - EC 3.1.3.5 (5'-Nucleotidase)
RN  - K72T3FS567 (Adenosine)
SB  - IM
MH  - 5'-Nucleotidase/deficiency/immunology/*metabolism
MH  - Adenosine/immunology
MH  - Adenosine Triphosphate/metabolism
MH  - Animals
MH  - Aorta/enzymology
MH  - Collagen/immunology
MH  - Constriction
MH  - Disease Models, Animal
MH  - Fibrosis/enzymology
MH  - Heart Failure/genetics/*immunology
MH  - Inflammation/*immunology
MH  - Interleukin-3/metabolism
MH  - Male
MH  - Mice
MH  - Mice, Knockout
MH  - Signal Transduction/*immunology
MH  - T-Lymphocytes/*immunology
OTO - NOTNLM
OT  - 5'-nucleotidase
OT  - collagen
OT  - heart failure
OT  - inflammation
OT  - receptors, purinergic P1
EDAT- 2017/04/14 06:00
MHDA- 2017/04/19 06:00
CRDT- 2017/04/14 06:00
PHST- 2016/06/13 [received]
PHST- 2017/03/16 [accepted]
AID - CIRCHEARTFAILURE.116.003346 [pii]
AID - 10.1161/CIRCHEARTFAILURE.116.003346 [doi]
PST - ppublish
SO  - Circ Heart Fail. 2017 Apr;10(4). pii: e003346. doi:
      10.1161/CIRCHEARTFAILURE.116.003346.

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