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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Circulation
2016 ; 134
(2
): 153-67
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Leukocyte-Expressed ?2-Adrenergic Receptors Are Essential for Survival After
Acute Myocardial Injury
#MMPMID27364164
Grisanti LA
; Gumpert AM
; Traynham CJ
; Gorsky JE
; Repas AA
; Gao E
; Carter RL
; Yu D
; Calvert JW
; García AP
; Ibáñez B
; Rabinowitz JE
; Koch WJ
; Tilley DG
Circulation
2016[Jul]; 134
(2
): 153-67
PMID27364164
show ga
BACKGROUND: Immune cell-mediated inflammation is an essential process for
mounting a repair response after myocardial infarction (MI). The sympathetic
nervous system is known to regulate immune system function through ?-adrenergic
receptors (?ARs); however, their role in regulating immune cell responses to
acute cardiac injury is unknown. METHODS: Wild-type (WT) mice were irradiated
followed by isoform-specific ?AR knockout (?ARKO) or WT bone-marrow
transplantation (BMT) and after full reconstitution underwent MI surgery.
Survival was monitored over time, and alterations in immune cell infiltration
after MI were examined through immunohistochemistry. Alterations in splenic
function were identified through the investigation of altered adhesion receptor
expression. RESULTS: ?2ARKO BMT mice displayed 100% mortality resulting from
cardiac rupture within 12 days after MI compared with ?20% mortality in WT BMT
mice. ?2ARKO BMT mice displayed severely reduced post-MI cardiac infiltration of
leukocytes with reciprocally enhanced splenic retention of the same immune cell
populations. Splenic retention of the leukocytes was associated with an increase
in vascular cell adhesion molecule-1 expression, which itself was regulated via
?-arrestin-dependent ?2AR signaling. Furthermore, vascular cell adhesion
molecule-1 expression in both mouse and human macrophages was sensitive to ?2AR
activity, and spleens from human tissue donors treated with ?-blocker showed
enhanced vascular cell adhesion molecule-1 expression. The impairments in splenic
retention and cardiac infiltration of leukocytes after MI were restored to WT
levels via lentiviral-mediated re-expression of ?2AR in ?2ARKO bone marrow before
transplantation, which also resulted in post-MI survival rates comparable to
those in WT BMT mice. CONCLUSIONS: Immune cell-expressed ?2AR plays an essential
role in regulating the early inflammatory repair response to acute myocardial
injury by facilitating cardiac leukocyte infiltration.
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